Joseph Loscalzo

Summary

Affiliation: Boston University
Country: USA

Publications

  1. ncbi request reprint Nitric oxide insufficiency, platelet activation, and arterial thrombosis
    J Loscalzo
    Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA
    Circ Res 88:756-62. 2001
  2. ncbi request reprint L-arginine and atherothrombosis
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    J Nutr 134:2798S-2800S; discussion 2818S-2819S. 2004
  3. ncbi request reprint Functional polymorphisms in a candidate gene for atherothrombosis: unraveling the complex fabric of a polygenic phenotype
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118 2394, USA
    J Am Coll Cardiol 41:946-8. 2003
  4. ncbi request reprint Stem cells and regeneration of the cardiovascular system: facts, fictions, and uncertainties
    Joseph Loscalzo
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Blood Cells Mol Dis 32:97-9. 2004
  5. ncbi request reprint Genetic determinants of vascular oxidant stress and endothelial dysfunction
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and the Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Congest Heart Fail 11:73-9. 2005
  6. ncbi request reprint Proteomics in cardiovascular biology and medicine
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Circulation 108:380-3. 2003
  7. ncbi request reprint Oxidative stress in endothelial cell dysfunction and thrombosis
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Pathophysiol Haemost Thromb 32:359-60. 2002
  8. ncbi request reprint Oxidant stress: a key determinant of atherothrombosis
    J Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118, USA
    Biochem Soc Trans 31:1059-61. 2003
  9. pmc Aminoglycosides decrease glutathione peroxidase-1 activity by interfering with selenocysteine incorporation
    Diane E Handy
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 281:3382-8. 2006
  10. pmc Inflammation, endothelial injury, and persistent pulmonary hypertension in heterozygous BMPR2-mutant mice
    Yanli Song
    Cardiovascular Division, Dept of Medicine, Brigham and Women s Hosiptal and Harvard Medical School, 77 Ave Louis Pasteur, NRB 630, Boston, MA 02115, USA
    Am J Physiol Heart Circ Physiol 295:H677-90. 2008

Detail Information

Publications104 found, 100 shown here

  1. ncbi request reprint Nitric oxide insufficiency, platelet activation, and arterial thrombosis
    J Loscalzo
    Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA
    Circ Res 88:756-62. 2001
    ..The complex biochemical reactions that underlie the function and inactivation of NO in the vasculature represent an important set of targets for therapeutic intervention for the prevention and treatment of arterial thrombotic disorders...
  2. ncbi request reprint L-arginine and atherothrombosis
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    J Nutr 134:2798S-2800S; discussion 2818S-2819S. 2004
    ..The interrelationships among these effects of L-arginine are reviewed here, and the potential benefits and risks of L-arginine supplementation are discussed...
  3. ncbi request reprint Functional polymorphisms in a candidate gene for atherothrombosis: unraveling the complex fabric of a polygenic phenotype
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118 2394, USA
    J Am Coll Cardiol 41:946-8. 2003
  4. ncbi request reprint Stem cells and regeneration of the cardiovascular system: facts, fictions, and uncertainties
    Joseph Loscalzo
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Blood Cells Mol Dis 32:97-9. 2004
    ....
  5. ncbi request reprint Genetic determinants of vascular oxidant stress and endothelial dysfunction
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and the Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Congest Heart Fail 11:73-9. 2005
    ..The relevance of deficiencies in glutathione peroxidase and glucose-6-phosphate dehydrogenase on endothelial and myocardial dysfunction will be reviewed...
  6. ncbi request reprint Proteomics in cardiovascular biology and medicine
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Circulation 108:380-3. 2003
  7. ncbi request reprint Oxidative stress in endothelial cell dysfunction and thrombosis
    Joseph Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Pathophysiol Haemost Thromb 32:359-60. 2002
    ..Selected antioxidants improve intracellular redox state and reverse ECD by improving the bioavailability of NO. These observations provide mechanistic insights into the molecular basis of ECD in vascular disease and its treatment...
  8. ncbi request reprint Oxidant stress: a key determinant of atherothrombosis
    J Loscalzo
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118, USA
    Biochem Soc Trans 31:1059-61. 2003
    ..The consequences of acquired and inherited deficiencies of these antioxidant enzymes for vascular oxidant stress, endothelial dysfunction and atherothrombosis will be reviewed...
  9. pmc Aminoglycosides decrease glutathione peroxidase-1 activity by interfering with selenocysteine incorporation
    Diane E Handy
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 281:3382-8. 2006
    ..These data show that G418 can affect the biosynthesis of this key antioxidant enzyme by promoting substitution at the UGA codon...
  10. pmc Inflammation, endothelial injury, and persistent pulmonary hypertension in heterozygous BMPR2-mutant mice
    Yanli Song
    Cardiovascular Division, Dept of Medicine, Brigham and Women s Hosiptal and Harvard Medical School, 77 Ave Louis Pasteur, NRB 630, Boston, MA 02115, USA
    Am J Physiol Heart Circ Physiol 295:H677-90. 2008
    ..Greater endothelial injury and an enhanced inflammatory response could be the underlying causes of the sensitivity and may work in concert with BMPR2 heterozygosity to promote the development of persistent pulmonary hypertension...
  11. pmc Increasing glucose 6-phosphate dehydrogenase activity restores redox balance in vascular endothelial cells exposed to high glucose
    Zhaoyun Zhang
    Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA
    PLoS ONE 7:e49128. 2012
    ..These studies illustrate that increasing G6PD activity restores redox balance in endothelial cells exposed to high glucose, which is a potentially important therapeutic target to protect ECs from the deleterious effects of high glucose...
  12. pmc Glutathione peroxidase-1 regulates mitochondrial function to modulate redox-dependent cellular responses
    Diane E Handy
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:11913-21. 2009
    ..Taken together, these data suggest that GPx-1 can modulate redox-dependent cellular responses by regulating mitochondrial function...
  13. ncbi request reprint Increased myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase
    Mohit Jain
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Circulation 109:898-903. 2004
    ..We therefore hypothesized that G6PD is essential for maintaining GSH levels and protecting the heart during ischemia-reperfusion injury...
  14. pmc Aldosterone inactivates the endothelin-B receptor via a cysteinyl thiol redox switch to decrease pulmonary endothelial nitric oxide levels and modulate pulmonary arterial hypertension
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, 75 Francis St, PBB 1, Boston, MA 02115, USA
    Circulation 126:963-74. 2012
    ..We hypothesized that aldosterone modulates PAH by disrupting ET(B)-eNOS signaling through a mechanism involving increased pulmonary endothelial oxidant stress...
  15. pmc Glutathione peroxidase-3 deficiency promotes platelet-dependent thrombosis in vivo
    Richard C Jin
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circulation 123:1963-73. 2011
    ..A deficiency of this enzyme has been associated with platelet-dependent thrombosis, and a promoter haplotype with reduced function has been associated with stroke risk...
  16. ncbi request reprint Heterozygous cellular glutathione peroxidase deficiency in the mouse: abnormalities in vascular and cardiac function and structure
    Marc A Forgione
    Evans Department of Medicine, Boston University School of Medicine, Boston, Mass, USA
    Circulation 106:1154-8. 2002
    ..Cellular GPx (GPx-1) is the principal intracellular isoform of GPx. We hypothesized that GPx-1 deficiency per se induces endothelial dysfunction and structural vascular abnormalities through increased oxidant stress...
  17. ncbi request reprint The combined effect of paraoxonase promoter and coding region polymorphisms on the risk of arterial ischemic stroke among young adults
    Barbara Voetsch
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, MA 02118, USA
    Arch Neurol 61:351-6. 2004
    ..Interindividual variability in PON1 levels is determined by the Q192R and L55M coding region polymorphisms and by 2 recently described polymorphisms in the promoter of the PON1 gene, C(-107)T and G(-824)A...
  18. pmc Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:7665-72. 2009
    ..These findings demonstrate that pathophysiologically relevant concentrations of aldosterone increase oxidant stress to convert GC to an NO(.)-insensitive state, resulting in disruption of normal vasodilatory signaling pathways in VSMC...
  19. pmc Promoter polymorphisms in the plasma glutathione peroxidase (GPx-3) gene: a novel risk factor for arterial ischemic stroke among young adults and children
    Barbara Voetsch
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, MA, USA
    Stroke 38:41-9. 2007
    ..The aim of this study is to identify polymorphisms in the GPx-3 gene, examine their relationship to arterial ischemic stroke (AIS) in a large series of children and young adults, and determine their functional molecular consequences...
  20. pmc Glucose-6-phosphate dehydrogenase-deficient mice have increased renal oxidative stress and increased albuminuria
    Yizhen Xu
    Renal Division, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    FASEB J 24:609-16. 2010
    ..These results show that decreased G6PD activity per se is sufficient to cause changes similar to those seen in diabetic mice...
  21. ncbi request reprint Sickle cell anemia is associated with reduced nitric oxide bioactivity in peripheral conduit and resistance vessels
    Robert T Eberhardt
    Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118 2393, USA
    Am J Hematol 74:104-11. 2003
    ..Resistance vessels have preserved response to exogenous NO donors but have diminished contribution of NO to endothelium-dependent vasodilation. Conduit vessels demonstrate impaired vasodilation to endogenous and exogenous NO...
  22. pmc Cardiomyogenesis in the aging and failing human heart
    Jan Kajstura
    Department of Anesthesia, Division of Cardiovascular Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circulation 126:1869-81. 2012
    ....
  23. pmc Homocysteine induces cardiomyocyte dysfunction and apoptosis through p38 MAPK-mediated increase in oxidant stress
    Xu Wang
    Department of Medicine, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
    J Mol Cell Cardiol 52:753-60. 2012
    ..Thus, Hcy may increase the risk for CVD not only by causing endothelial dysfunction, but also by directly exerting detrimental effects on cardiomyocytes...
  24. ncbi request reprint L-Homocysteine and L-homocystine stereospecifically induce endothelial nitric oxide synthase-dependent lipid peroxidation in endothelial cells
    Stanley J Heydrick
    Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University, School of Medicine, Boston, MA 02118, USA
    Free Radic Biol Med 36:632-40. 2004
    ..Thus, homocyst(e)ine actively promotes oxidative stress in endothelial cells via an eNOS-dependent mechanism...
  25. pmc Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression
    Edith Lubos
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    FASEB J 24:2525-32. 2010
    ..Taken together, these data suggest that GPx-1 modulates the endothelial cell response to LPS, in part, by altering CD14-mediated effects...
  26. pmc Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity
    Jane A Leopold
    Whitaker Cardiovascular Institute, 700 Albany Street, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Nat Med 13:189-97. 2007
    ..These findings demonstrate that aldosterone induces a G6PD-deficient phenotype to impair endothelial function; aldosterone antagonism or gene transfer of G6pd improves vascular reactivity by restoring G6PD activity...
  27. pmc Impaired angiogenesis in glutathione peroxidase-1-deficient mice is associated with endothelial progenitor cell dysfunction
    Gennaro Galasso
    Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Circ Res 98:254-61. 2006
    ..These data suggest that EPC dysfunction is a mechanism by which elevated levels of ROS can contribute to vascular disease...
  28. ncbi request reprint Glucose-6-phosphate dehydrogenase deficiency decreases vascular superoxide and atherosclerotic lesions in apolipoprotein E(-/-) mice
    Reiko Matsui
    Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Arterioscler Thromb Vasc Biol 26:910-6. 2006
    ..The purpose of this study was to examine whether G6PD deficiency affects vascular oxidants and atherosclerosis in high-fat fed apolipoprotein (apo) E(-/-) mice...
  29. ncbi request reprint Role of promoter polymorphisms in the plasma glutathione peroxidase (GPx-3) gene as a risk factor for cerebral venous thrombosis
    Barbara Voetsch
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02115, USA
    Stroke 39:303-7. 2008
    ..We recently identified a haplotype (H(2)) in the GPx-3 gene promoter that increases the risk of arterial ischemic stroke among children and young adults...
  30. ncbi request reprint Glucose-6-phosphate dehydrogenase modulates cytosolic redox status and contractile phenotype in adult cardiomyocytes
    Mohit Jain
    Cardiac Muscle Research Laboratory, Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass, USA
    Circ Res 93:e9-16. 2003
    ..The full text of this article is available online at http://www.circresaha.org...
  31. pmc The critical roles of platelet activation and reduced NO bioavailability in fatal pulmonary arterial hypertension in a murine hemolysis model
    Weiguo Hu
    Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Blood 116:1613-22. 2010
    ..These findings further highlight the importance of the inhibition of platelet activation and the enhancement of NO bioavailability for the treatment and prevention of hemolysis-associated (fatal) PAH...
  32. pmc Selenistasis: epistatic effects of selenium on cardiovascular phenotype
    Jacob Joseph
    Department of Medicine, VA Boston Healthcare System, Boston, MA 02132, USA
    Nutrients 5:340-58. 2013
    ..Given the complexity of selenium biology, systems biology approaches may be necessary to reach the goal of optimization of selenium status to promote health and prevent disease...
  33. ncbi request reprint Cellular glutathione peroxidase deficiency and endothelial dysfunction
    Marc A Forgione
    Evans Department of Medicine, Boston, Massachusetts 02118, USA
    Am J Physiol Heart Circ Physiol 282:H1255-61. 2002
    ..These vascular abnormalities can be attenuated by increasing bioavailable intracellular thiol pools...
  34. pmc Tracking chromatid segregation to identify human cardiac stem cells that regenerate extensively the infarcted myocardium
    Jan Kajstura
    Departments of Anesthesia and Medicine, Division of Cardiovascular Medicine, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    Circ Res 111:894-906. 2012
    ....
  35. doi request reprint The effect of salt on renal damage in eNOS-deficient mice
    Geraldine Daumerie
    Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA
    Hypertens Res 33:170-6. 2010
    ..001 vs. normal salt diet). eNOS(-/-) mice may be used as a model of salt-induced and hypertension-associated renal injury as seen in African Americans...
  36. pmc Both maximal expression of selenoproteins and selenoprotein deficiency can promote development of type 2 diabetes-like phenotype in mice
    Vyacheslav M Labunskyy
    Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    Antioxid Redox Signal 14:2327-36. 2011
    ..These findings indicate that both high expression of selenoproteins and selenoprotein deficiency may dysregulate glucose homeostasis and suggest a role for selenoproteins in development of diabetes...
  37. pmc High glucose inhibits glucose-6-phosphate dehydrogenase, leading to increased oxidative stress and beta-cell apoptosis
    Zhaoyun Zhang
    Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    FASEB J 24:1497-505. 2010
    ..G6PD plays an important role in beta-cell function and survival. High-glucose-mediated decrease in G6PD activity may provide a mechanistic explanation for the gradual loss of beta cells in patients with diabetes...
  38. doi request reprint Balancing role of nitric oxide in complement-mediated activation of platelets from mCd59a and mCd59b double-knockout mice
    Xuebin Qin
    Department of Medicine, Brigham and Women s Hospital, Boston, Massachusetts, USA
    Am J Hematol 84:221-7. 2009
    ..These results indicate that the thrombotic diathesis of PNH patients could be due to a combination of increased complement-mediated platelet activation and reduced NO-bioavailability as a consequence of hemolysis...
  39. pmc Methoxistasis: integrating the roles of homocysteine and folic acid in cardiovascular pathobiology
    Jacob Joseph
    Department of Medicine, VA Boston Healthcare System, Boston, MA 02132, USA
    Nutrients 5:3235-56. 2013
    ..This approach could lead to significant advances in preventing and treating cardiovascular diseases, including heart failure. ..
  40. ncbi request reprint Systems analysis of oxidant stress in the vasculature
    Diane E Handy
    Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    IUBMB Life 65:911-20. 2013
    ....
  41. pmc Increased susceptibility to pulmonary hypertension in heterozygous BMPR2-mutant mice
    Yanli Song
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Boston, MA, USA
    Circulation 112:553-62. 2005
    ..To understand the role of BMPR2 in the development of IPAH, we examined the phenotype of BMPR2(+/-) mice and their response to inflammatory stress...
  42. pmc S-nitrosothiols and the S-nitrosoproteome of the cardiovascular system
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Antioxid Redox Signal 18:270-87. 2013
    ....
  43. pmc Plasma aldosterone levels are elevated in patients with pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study
    Bradley A Maron
    Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Eur J Heart Fail 15:277-83. 2013
    ..Thus, the central aim of the current study is to determine if hyperaldosteronism is an unrecognized component of the PAH clinical syndrome...
  44. pmc Regulation of the extracellular antioxidant selenoprotein plasma glutathione peroxidase (GPx-3) in mammalian cells
    Filomena G Ottaviano
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, MA, USA
    Mol Cell Biochem 327:111-26. 2009
    ..Selenocompound supplementation and co-transfection with SECIS binding protein 2 increased wild type rGPx-3 expression. These results demonstrate the importance of translational mechanisms in GPx-3 expression...
  45. pmc Glutathione peroxidase-1 deficiency augments proinflammatory cytokine-induced redox signaling and human endothelial cell activation
    Edith Lubos
    Department of Medicine, Cardiovascular Division, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:35407-17. 2011
    ..Targeted DUSP4 knockdown enhanced TNF-α-mediated ERK1/2 pathway activation and resulted in increased adhesion molecule expression, indicating that GPx-1 deficiency may augment TNF-α-mediated events, in part, by regulating DUSP4...
  46. ncbi request reprint Usefulness of the aldosterone synthase gene polymorphism C-344-T to predict cardiac remodeling in African-Americans versus non-African-Americans with chronic systolic heart failure
    Andreia Biolo
    Cardiovascular Section and Evans Department of Medicine, Boston University School of Public Health, Boston, Massachusetts, USA
    Am J Cardiol 100:285-90. 2007
    ..Although this genetic-driven increase in aldosterone activity should predispose to worse cardiac remodeling, it may represent a more susceptible state and enhanced response to therapy in this racial subgroup...
  47. ncbi request reprint Glucose-6-phosphate dehydrogenase modulates vascular endothelial growth factor-mediated angiogenesis
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 278:32100-6. 2003
    ..These findings demonstrate that G6PD modulates angiogenesis and may represent a novel angiogenic regulator...
  48. ncbi request reprint Nitric oxide insufficiency and atherothrombosis
    Barbara Voetsch
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, 715 Albany Street, W507, Boston, MA 02118, USA
    Histochem Cell Biol 122:353-67. 2004
    ....
  49. pmc The effect of L-arginine and creatine on vascular function and homocysteine metabolism
    Eiman Jahangir
    Boston University School of Medicine, Boston, MA 02118, USA
    Vasc Med 14:239-48. 2009
    ..The unexpected increase in homocysteine levels following creatine supplementation could have adverse effects and merits further study, since creatine is a commonly used dietary supplement...
  50. ncbi request reprint Glucose-6-phosphate dehydrogenase overexpression decreases endothelial cell oxidant stress and increases bioavailable nitric oxide
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 700 Albany St CABR W 507, Boston, MA 02118, USA
    Arterioscler Thromb Vasc Biol 23:411-7. 2003
    ..Therefore, we examined whether overexpression of G6PD would decrease reactive oxygen species accumulation and increase bioavailable NO. in endothelial cells...
  51. pmc Regulation of the protein disulfide proteome by mitochondria in mammalian cells
    Yi Yang
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:10813-7. 2007
    ..These data support the concept of two subproteomes comprising the disulfide proteome, a structural group and a redox-sensitive regulatory group, with the latter having direct functional consequences for the cell...
  52. pmc Bone morphogenetic protein-2 activates NADPH oxidase to increase endoplasmic reticulum stress and human coronary artery smooth muscle cell calcification
    Marcel Liberman
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Biochem Biophys Res Commun 413:436-41. 2011
    ..Thus, in HCSMC, BMP-2 increases oxidant stress and ER stress to increase Runx2 expression and promote vascular smooth muscle cell calcification...
  53. ncbi request reprint Homocysteine and glutathione peroxidase-1
    Edith Lubos
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    Antioxid Redox Signal 9:1923-40. 2007
    ....
  54. pmc Effectiveness of spironolactone plus ambrisentan for treatment of pulmonary arterial hypertension (from the [ARIES] study 1 and 2 trials)
    Bradley A Maron
    Veterans Affairs Boston Healthcare System, Department of Cardiology, 1400 VFW, Parkway, Boston, MA, USA
    Am J Cardiol 112:720-5. 2013
    ..In conclusion, these pilot data suggest that coupling spironolactone and endothelin type-A receptor antagonism may be clinically beneficial in PAH. Prospective clinical trials are required to further characterize our findings...
  55. pmc High-resolution imaging of selenium in kidneys: a localized selenium pool associated with glutathione peroxidase 3
    Mikalai Malinouski
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts, USA
    Antioxid Redox Signal 16:185-92. 2012
    ..In this work, we applied high-resolution synchrotron X-ray fluorescence microscopy (XFM) to map selenium distribution in mouse liver and kidney...
  56. pmc Role of oxidative stress and nitric oxide in atherothrombosis
    Edith Lubos
    Department of Medicine, Brigham and Women s Hospital, and Harvard Medical School, Boston, Massachusetts 02115, USA
    Front Biosci 13:5323-44. 2008
    ..This review examines the role of oxidative stress and NO in mechanisms of endothelial and vascular dysfunction with an emphasis on atherothrombosis...
  57. pmc MicroRNA-210 controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2
    Stephen Y Chan
    Division of Cardiology, Department of Medicine, Massachusetts General Hospital, Boston, MA 02114, USA
    Cell Metab 10:273-84. 2009
    ..These results identify important mechanistic connections among microRNA, iron-sulfur cluster biology, hypoxia, and mitochondrial function, with broad implications for cellular metabolism and adaptation to cellular stress...
  58. pmc Elevated levels of homocysteine compromise blood-brain barrier integrity in mice
    Atul F Kamath
    CBR Institute for Biomedical Research, 800 Huntington Ave, Boston, MA 02115, USA
    Blood 107:591-3. 2006
    ..Our study suggests an important toxic effect of elevated Hcy on brain microvessels and implicates Hcy in the disruption of the BBB...
  59. ncbi request reprint Adenosine-dependent induction of glutathione peroxidase 1 in human primary endothelial cells and protection against oxidative stress
    Yufeng Zhang
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Circ Res 96:831-7. 2005
    ..These data suggest that adenosine may protect the cardiovascular system from ischemia/reperfusion injury, in part, by enhancing the expression of the central intracellular antioxidant enzyme, GPx-1...
  60. ncbi request reprint Homocysteine and atherothrombosis: diagnosis and treatment
    Diane E Handy
    Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA
    Curr Atheroscler Rep 5:276-83. 2003
    ..However, several recent studies suggest a benefit for reduction of plasma homocysteine levels, as individuals with lower homocysteine have reduced cardiovascular event rates...
  61. ncbi request reprint Hypoxia potentiates nitric oxide-mediated apoptosis in endothelial cells via peroxynitrite-induced activation of mitochondria-dependent and -independent pathways
    Geoffrey A Walford
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 279:4425-32. 2004
    ..These findings confirm that high flux of NO* under hypoxic conditions promotes cell death via mitochondrial damage and mitochondrial-independent mechanisms by peroxynitrite...
  62. ncbi request reprint Glucose-6 phosphate dehydrogenase deficiency decreases the vascular response to angiotensin II
    Reiko Matsui
    Vascular Biology Unit, Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118 2393, USA
    Circulation 112:257-63. 2005
    ..We determined the hypertensive and vascular hypertrophic response to Ang II in G6PD-deficient mice...
  63. ncbi request reprint Effect of 5-lipoxygenase on the development of pulmonary hypertension in rats
    John E Jones
    Department of Surgery, Boston University School of Medicine, Boston, MA 02118, USA
    Am J Physiol Heart Circ Physiol 286:H1775-84. 2004
    ..These data suggest that 5-LO plays a critical role in the progression of pulmonary hypertension in rats and that the detrimental effect of 5-LO is manifest only in the setting of pulmonary vascular endothelial cell dysfunction...
  64. ncbi request reprint Homocysteine down-regulates cellular glutathione peroxidase (GPx1) by decreasing translation
    Diane E Handy
    Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 280:15518-25. 2005
    ..These data support the conclusion that homocysteine decreases GPx1 activity by altering the translational mechanism essential for the synthesis of this selenocysteine-containing protein...
  65. ncbi request reprint Determinants of human plasma glutathione peroxidase (GPx-3) expression
    Charlene Bierl
    Whitaker Cardiovascular Institute and the Evans Department of Medicine, Boston, MA 02118, USA
    J Biol Chem 279:26839-45. 2004
    ..These results demonstrate the presence of a novel functional transcription start site for the human GPx-3 gene with a promoter regulated by hypoxia, and identify unique translational determinants of GPx-3 expression...
  66. pmc Oxidative risk for atherothrombotic cardiovascular disease
    Jane A Leopold
    Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Free Radic Biol Med 47:1673-706. 2009
    ....
  67. ncbi request reprint Different effects of angiotensin receptor blockade on end-organ damage in salt-dependent and salt-independent hypertension
    Karlene Maitland
    Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass, USA
    Circulation 114:905-11. 2006
    ..Although angiotensin II type 1 receptor blockers have emerged as effective antihypertensive agents, it is not known how efficacious these agents are in treating hypertension-associated target organ damage...
  68. ncbi request reprint Redox regulation in the extracellular environment
    Filomena G Ottaviano
    Whitaker Cardiovascular Institute, MA, USA
    Circ J 72:1-16. 2008
    ....
  69. ncbi request reprint Nitric oxide and posttranslational modification of the vascular proteome: S-nitrosation of reactive thiols
    Diane E Handy
    Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Arterioscler Thromb Vasc Biol 26:1207-14. 2006
    ..These findings suggest the utility of using proteomic methods to identify unique targets for protein S-nitrosation to understand further the molecular mechanisms of the effects of NO*...
  70. ncbi request reprint Should hyperhomocysteinemia be treated in patients with atherosclerotic disease?
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Curr Atheroscler Rep 9:375-83. 2007
    ..However, the role of folic acid therapy in patients with intermediate or severe hyperhomocysteinemia, or for primary prevention of cardiovascular diseases, remains unresolved...
  71. ncbi request reprint Ozone--from environmental pollutant to atherogenic determinant
    Joseph Loscalzo
    Boston University School of Medicine, Boston, USA
    N Engl J Med 350:834-5. 2004
  72. ncbi request reprint The effect of angiotensin-converting enzyme inhibition on endothelial function and oxidant stress
    Anne Ward Scribner
    Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA
    Eur J Pharmacol 482:95-9. 2003
    ..The biochemical basis for this protective mechanism is not entirely clear; however, these actions suggest that zofenopril may reduce endothelial effects of risk factors for atherothrombotic disease...
  73. pmc Redox Pioneer: Professor Joseph Loscalzo
    Jane A Leopold
    Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Antioxid Redox Signal 13:1125-32. 2010
    Dr. Joseph Loscalzo (M.D., 1978; Ph.D...
  74. pmc Reciprocal regulation of 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression by dexamethasone inhibits human coronary artery smooth muscle cell proliferation in vitro
    George Michas
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0630 K, Boston, MA 02115, USA
    Mol Cell Biochem 346:69-79. 2011
    ..These findings suggest that 11β-HSD1 plays a role in the effects of glucocorticoids on vascular smooth muscle cell phenotype...
  75. pmc Expression of 5-lipoxygenase in pulmonary artery endothelial cells
    Ying Yi Zhang
    Whitaker Cardiovascular Institute, and Evans Department of Medicine, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA
    Biochem J 361:267-76. 2002
    ..However, increased expression of 5LO in PAECs can lead to the production of all downstream leukotrienes, which could potentially cause endothelial dysfunction in the pulmonary vasculature...
  76. ncbi request reprint Cellular redox state and endothelial dysfunction in mildly hyperhomocysteinemic cystathionine beta-synthase-deficient mice
    Norbert Weiss
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118 2394, USA
    Arterioscler Thromb Vasc Biol 22:34-41. 2002
    ..These findings emphasize the importance of intracellular redox balance for nitric oxide bioactivity and endothelial function...
  77. ncbi request reprint 5-Lipoxygenase and human pulmonary artery endothelial cell proliferation
    Jennifer L Walker
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Am J Physiol Heart Circ Physiol 282:H585-93. 2002
    ..3-5 microM). These data show that 5LO inhibitors impaired the proliferative response of the cultured PAECs, suggesting that this enzyme may contribute to PAEC growth under certain pathological conditions...
  78. ncbi request reprint Prevention of hypertension and renal dysfunction in Dahl rats by alpha-tocopherol
    Patrick Forde
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Massachusetts 02118, USA
    J Cardiovasc Pharmacol 42:82-8. 2003
    ....
  79. doi request reprint Membrane redox state and apoptosis: death by peroxide
    Joseph Loscalzo
    Department of Medicine, Brigham and Women s Hospital, 75 Francis Street, Harvard Medical School, Boston, MA 02118 2394, USA
    Cell Metab 8:182-3. 2008
    ..In this issue of Cell Metabolism, Seiler et al. (2008) show that a lipid oxidase, 12/15-lipoxygenase, and a membrane antioxidant enzyme, glutathione peroxidase-4, interact to regulate a novel redox-dependent cell death pathway...
  80. ncbi request reprint Homocysteine
    Bradley A Maron
    Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    Clin Lab Med 26:591-609, vi. 2006
    ..Although new technologies have been developed over the past 2 decades that have enhanced the precision of measurement, universal guidelines for circulating homocysteine determination remain lacking...
  81. ncbi request reprint Effects of black race on forearm resistance vessel function
    David F Kahn
    Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass, USA
    Hypertension 40:195-201. 2002
    ..Further studies will be required to elucidate the mechanisms and determine whether these insights will lead to more appropriately tailored management of hypertension and its complications...
  82. ncbi request reprint Cyclooxygenase inhibition and cardiovascular risk
    Elliott M Antman
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
    Circulation 112:759-70. 2005
  83. ncbi request reprint Endogenous mechanisms of inhibition of platelet function
    Richard C Jin
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, MA 02118, USA
    Microcirculation 12:247-58. 2005
    ..Each of these factors is discussed in turn, and the specific mechanisms by which they inhibit platelet function are reviewed...
  84. ncbi request reprint Genetics of thrombophilia: impact on atherogenesis
    Barbara Voetsch
    Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Curr Opin Lipidol 15:129-43. 2004
    ..The goal of this review is to present an update on basic and epidemiological findings associating variants in prothrombotic genes with atherogenesis and atherothrombotic disease...
  85. ncbi request reprint Oxidative enzymopathies and vascular disease
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Arterioscler Thromb Vasc Biol 25:1332-40. 2005
    ..Individually, each of these polymorphisms imposes a state of uncompensated oxidant stress on the vasculature and collectively comprise the oxidative enzymopathies...
  86. ncbi request reprint Pulmonary arterial hypertension
    Harrison W Farber
    Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    N Engl J Med 351:1655-65. 2004
  87. pmc S-nitrosoprotein formation and localization in endothelial cells
    Yi Yang
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Proc Natl Acad Sci U S A 102:117-22. 2005
    ..These data offer methods and insights into identifying the protein targets of S-nitrosation reactions and their potential role in cell function and phenotype...
  88. ncbi request reprint Atherosclerotic Vascular Disease Conference: Writing Group III: pathophysiology
    David P Faxon
    Circulation 109:2617-25. 2004
  89. ncbi request reprint Vasoactive substances: nitric oxide and endothelial dysfunction in atherosclerosis
    Guilia Russo
    University of Padua, Padua, Italy
    Vascul Pharmacol 38:259-69. 2002
    ..Strategies to replenish bioavailable NO include the administration of organic nitrosovasodilators or NO donor compounds, therapies to improve NO synthase function, and gene therapy...
  90. ncbi request reprint Adverse effects of supplemental L-arginine in atherosclerosis: consequences of methylation stress in a complex catabolism?
    Joseph Loscalzo
    Arterioscler Thromb Vasc Biol 23:3-5. 2003
  91. ncbi request reprint Discovering the full spectrum of cardiovascular disease: Minority Health Summit 2003: report of the Basic Science Writing Group
    Ivor J Benjamin
    Circulation 111:e120-3. 2005
  92. ncbi request reprint Endothelial dysfunction and atherothrombosis in mild hyperhomocysteinemia
    Norbert Weiss
    Medical Policlinic, Division of Angiology, University Hospital, Innenstadt, Munich, Germany
    Vasc Med 7:227-39. 2002
    ....
  93. ncbi request reprint Influence of hyperhomocysteinemia on the cellular redox state--impact on homocysteine-induced endothelial dysfunction
    Norbert Weiss
    Medizinische Poliklinik Innenstadt, Klinikum der Universitat Munchen, Munich, Germany
    Clin Chem Lab Med 41:1455-61. 2003
    ..Taken together, these findings strongly suggest that the adverse vascular effects of homocysteine are at least partly mediated by oxidative inactivation of nitric oxide...
  94. ncbi request reprint Molecular mechanisms underlying the proangiogenic effect of factor XIII
    Rima Dardik
    Institute of Thrombosis and Hemostasis, Sheba Medical Center, Tel Hashomer, Israel
    Arterioscler Thromb Vasc Biol 25:526-32. 2005
    ..The aim of this study was to elucidate the molecular events underlying the proangiogenic effects of activated FXIII (FXIIIa) on human umbilical vein endothelial cells (HUVECs)...
  95. pmc Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice
    Namakkal S Rajasekaran
    Center for Cardiovascular Translational Biomedicine, Division of Cardiology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
    Cell 130:427-39. 2007
    ..These findings demonstrate that dysregulation of G6PD activity is necessary and sufficient for maladaptive reductive stress and suggest a novel therapeutic target for abrogating R120GCryAB cardiomyopathy and heart failure in humans...
  96. ncbi request reprint Glycoxidized low-density lipoprotein downregulates endothelial nitricoxide synthase in human coronary cells
    Claudio Napoli
    Department of Medicine 0682, University of California, San Diego, California 92093, USA
    J Am Coll Cardiol 40:1515-22. 2002
    ..We examined the hypothesis that low-density lipoprotein (LDL) that is both oxidized and glycosylated potently downregulates the expression of endothelial nitric oxide synthase III (NOSIII) in human coronary endothelial cells...
  97. ncbi request reprint Nitric oxide donors and cardiovascular agents modulating the bioactivity of nitric oxide: an overview
    Louis J Ignarro
    Nitric Oxide Research Group, Molecular and Medical Pharmacology, Center for the Health Sciences, University of California, Los Angeles, USA
    Circ Res 90:21-8. 2002
    ..Here, we review these classes of agents, summarizing their fundamental chemistry and pharmacology, and provide an overview of their cardiovascular mechanisms of action...
  98. ncbi request reprint Shouldering the risk factor burden: infection, atherosclerosis, and the vascular endothelium
    Joseph A Vita
    Circulation 106:164-6. 2002
  99. ncbi request reprint Homocysteine trials--clear outcomes for complex reasons
    Joseph Loscalzo
    N Engl J Med 354:1629-32. 2006
  100. ncbi request reprint Task Force on Strategic Research Direction: Basic Science Subgroup key science topics report
    Joseph Loscalzo
    Circulation 106:e149-61. 2002
  101. ncbi request reprint Association studies in an era of too much information: clinical analysis of new biomarker and genetic data
    Joseph Loscalzo
    Circulation 116:1866-70. 2007