Elizabeth Murphy

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Signaling by S-nitrosylation in the heart
    Elizabeth Murphy
    Cardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA Electronic address
    J Mol Cell Cardiol 73:18-25. 2014
  2. ncbi request reprint Unresolved questions from the analysis of mice lacking MCU expression
    Elizabeth Murphy
    Systems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA Electronic address
    Biochem Biophys Res Commun 449:384-5. 2014
  3. pmc Mechanism of cardioprotection: what can we learn from females?
    Elizabeth Murphy
    NHLBI, NIH, Room 8N202, Building 10, 10 Center Drive, Bethesda, MD, USA
    Pediatr Cardiol 32:354-9. 2011
  4. pmc Ion transport and energetics during cell death and protection
    Elizabeth Murphy
    National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
    Physiology (Bethesda) 23:115-23. 2008
  5. pmc Regulation of intracellular and mitochondrial sodium in health and disease
    Elizabeth Murphy
    Translational Medicine Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA
    Circ Res 104:292-303. 2009
  6. pmc Estrogen signaling and cardiovascular disease
    Elizabeth Murphy
    Cardiac Physiology Section, Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Circ Res 109:687-96. 2011
  7. pmc Does inhibition of glycogen synthase kinase protect in mice?
    Elizabeth Murphy
    Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA
    Circ Res 103:226-8. 2008
  8. pmc Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury
    Elizabeth Murphy
    Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
    Physiol Rev 88:581-609. 2008
  9. pmc Sex differences in the phosphorylation of mitochondrial proteins result in reduced production of reactive oxygen species and cardioprotection in females
    Claudia J Lagranha
    Translational Medicine Branch, NHLBI NIH 10 Center Bethesda, MD 20892, USA
    Circ Res 106:1681-91. 2010
  10. pmc CypD(-/-) hearts have altered levels of proteins involved in Krebs cycle, branch chain amino acid degradation and pyruvate metabolism
    Sara Menazza
    Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
    J Mol Cell Cardiol 56:81-90. 2013

Collaborators

Detail Information

Publications86

  1. ncbi request reprint Signaling by S-nitrosylation in the heart
    Elizabeth Murphy
    Cardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA Electronic address
    J Mol Cell Cardiol 73:18-25. 2014
    ..The specific mechanisms that regulate protein SNO, including redox-dependent processes, will also be discussed. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System". ..
  2. ncbi request reprint Unresolved questions from the analysis of mice lacking MCU expression
    Elizabeth Murphy
    Systems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA Electronic address
    Biochem Biophys Res Commun 449:384-5. 2014
    ..Here, we discuss our findings as well as potential explanations for some of the more unexpected results. ..
  3. pmc Mechanism of cardioprotection: what can we learn from females?
    Elizabeth Murphy
    NHLBI, NIH, Room 8N202, Building 10, 10 Center Drive, Bethesda, MD, USA
    Pediatr Cardiol 32:354-9. 2011
    ..It investigates estrogen signaling mediated by the nuclear estrogen receptors alpha and beta and the G-protein-coupled receptor (GPR 30/GPER). Estrogen signaling via nitric oxide and the PI3K pathway are discussed...
  4. pmc Ion transport and energetics during cell death and protection
    Elizabeth Murphy
    National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
    Physiology (Bethesda) 23:115-23. 2008
    ..This review will discuss mechanisms involved in alterations in ions and high energy phosphate metabolites in perfused or intact heart during ischemia and reperfusion...
  5. pmc Regulation of intracellular and mitochondrial sodium in health and disease
    Elizabeth Murphy
    Translational Medicine Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA
    Circ Res 104:292-303. 2009
    ..Although much has been learned about sodium regulation in the heart, there are still many unanswered questions, particularly concerning mitochondrial Na regulation...
  6. pmc Estrogen signaling and cardiovascular disease
    Elizabeth Murphy
    Cardiac Physiology Section, Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Circ Res 109:687-96. 2011
    ..This article reviews the different estrogen receptors and their signaling mechanisms, discusses mechanisms that regulate estrogen receptor levels and locations, and considers the cardiovascular effects of estrogen signaling...
  7. pmc Does inhibition of glycogen synthase kinase protect in mice?
    Elizabeth Murphy
    Vascular Medicine Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA
    Circ Res 103:226-8. 2008
  8. pmc Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury
    Elizabeth Murphy
    Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
    Physiol Rev 88:581-609. 2008
    ..Preconditioning activates a number of signaling pathways that reduce Ca(2+) overload and reduce activation of the mitochondrial permeability transition pore. The mitochondrial targets of cardioprotective signals are discussed in detail...
  9. pmc Sex differences in the phosphorylation of mitochondrial proteins result in reduced production of reactive oxygen species and cardioprotection in females
    Claudia J Lagranha
    Translational Medicine Branch, NHLBI NIH 10 Center Bethesda, MD 20892, USA
    Circ Res 106:1681-91. 2010
    ..Although premenopausal females have a lower risk for cardiovascular disease, the mechanism(s) are poorly understood...
  10. pmc CypD(-/-) hearts have altered levels of proteins involved in Krebs cycle, branch chain amino acid degradation and pyruvate metabolism
    Sara Menazza
    Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
    J Mol Cell Cardiol 56:81-90. 2013
    ..In summary, CypD(-/-) hearts exhibit changes in many metabolic pathways and caution should be used when interpreting results from these mice as due solely to inhibition of the MPTP...
  11. doi request reprint Cyclophilin D modulates mitochondrial acetylome
    Tiffany Tuyen M Nguyen
    From the Systems Biology Center T T M N, S M, J S, E M, Division of Cardiovascular Sciences R W, Proteomics Core Facility Y C, G W, M G, and Center for Molecular Medicine M N S, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD and Department of Pathology, Johns Hopkins Medical Center, Baltimore, MD C S
    Circ Res 113:1308-19. 2013
    ..As acetylation has been shown to regulate metabolism, we tested whether changes in protein acetylation might play a role in these metabolic changes in CypD(-/-) hearts...
  12. pmc The physiological role of mitochondrial calcium revealed by mice lacking the mitochondrial calcium uniporter
    Xin Pan
    1 Center for Molecular Medicine, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA 2 National Center of Biomedical Analysis, Beijing 100850, China 3
    Nat Cell Biol 15:1464-72. 2013
    ..Taken together, these results clarify how acute alterations in mitochondrial matrix calcium can regulate mammalian physiology. ..
  13. pmc Disruption of caveolae blocks ischemic preconditioning-mediated S-nitrosylation of mitochondrial proteins
    Junhui Sun
    Systems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Antioxid Redox Signal 16:45-56. 2012
    ..Mitochondria are key regulators of preconditioning, and most proteins showing an increase in SNO with IPC are mitochondrial. The aim of this study was to address how IPC transduces NO/SNO signaling to mitochondria in the heart...
  14. pmc Cardioprotection leads to novel changes in the mitochondrial proteome
    Renee Wong
    Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Am J Physiol Heart Circ Physiol 298:H75-91. 2010
    ..Thus the ability of PC and GSK inhibition to alter the expression levels of electron transport complexes will have important implications for mitochondrial function...
  15. pmc Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female rats
    Anne M Deschamps
    National Institutes of Health, National Heart, Lung, and Blood Institute, Translational Medicine Branch, Laboratory of Cardiac Physiology, Bethesda, MD 20892, USA
    Am J Physiol Heart Circ Physiol 297:H1806-13. 2009
    ..Taken together, the data show that G-1 activation of GPER improves functional recovery and reduces infarct size in isolated rat hearts following I/R through a PI3K-dependent, gender-independent mechanism...
  16. pmc Measurement of S-nitrosylation occupancy in the myocardium with cysteine-reactive tandem mass tags: short communication
    Mark J Kohr
    Laboratory of Cardiac Physiology, Systems Biology Center, National Heart Lung and Blood Institute, Bethesda, MD 20892, USA
    Circ Res 111:1308-12. 2012
    ..However, little is known with regard to the percentage of a given protein that is modified by SNO (ie, SNO occupancy). Current methods allow for the relative quantification of SNO levels, but not for the determination of SNO occupancy...
  17. ncbi request reprint Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transport
    Junhui Sun
    NHLBI, NIH, Vascular Medicine Branch, Bethesda, MD 20892, USA
    Circ Res 101:1155-63. 2007
    ..IPC and GSNO produced a similar pattern of S-nitrosylation modification and cardiac protection against ischemia/reperfusion injury, suggesting that protein S-nitrosylation may play an important cardioprotective role in heart...
  18. ncbi request reprint Transgenic expression of Bcl-2 modulates energy metabolism, prevents cytosolic acidification during ischemia, and reduces ischemia/reperfusion injury
    Kenichi Imahashi
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Circ Res 95:734-41. 2004
    ..Immunoprecipitation showed greater interaction between Bcl-2 and voltage-dependent anion channel during ischemia. These data indicate that Bcl-2 modulation of metabolism contributes to cardioprotection...
  19. ncbi request reprint Male/female differences in intracellular Na+ regulation during ischemia/reperfusion in mouse heart
    Kenichi Imahashi
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, RTP, NC 27709, USA
    J Mol Cell Cardiol 37:747-53. 2004
    ..Thus the data show that the sex difference in the [Na(+)](i) regulation is mediated through a NO-dependent mechanism, and the difference in susceptibility to I/R injury appears to result from a difference in Na(+) influx...
  20. pmc Acute inhibition of GSK causes mitochondrial remodeling
    Tiffany Nguyen
    Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
    Am J Physiol Heart Circ Physiol 302:H2439-45. 2012
    ..Taken together, these data show that SB leads to a remodeling of the mitochondrial proteome that is partially GD sensitive...
  21. pmc S-nitrosylation: a radical way to protect the heart
    Elizabeth Murphy
    Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA
    J Mol Cell Cardiol 52:568-77. 2012
    ..The role of nitric oxide synthase uncoupling in cardioprotection will also be addressed. This article is part of a Special Section entitled "Post-translational Modification."..
  22. ncbi request reprint Overexpression of the Na+/H+ exchanger and ischemia-reperfusion injury in the myocardium
    Kenichi Imahashi
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    Am J Physiol Heart Circ Physiol 292:H2237-47. 2007
    ..These results indicate that the basal activity of NHE1 is not rate limiting in causing damage during I/R, therefore, increasing the level of NHE1 does not enhance injury and can have some small protective effects...
  23. pmc Optical spectroscopy in turbid media using an integrating sphere: mitochondrial chromophore analysis during metabolic transitions
    David J Chess
    Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Anal Biochem 439:161-72. 2013
    ..Surprisingly, I/R resulted in an inhibition of all measured MOPC conductances, suggesting a coordinated down-regulation of mitochondrial activity with this well-established cardiac perturbation...
  24. pmc Essential role of nitric oxide in acute ischemic preconditioning: S-nitros(yl)ation versus sGC/cGMP/PKG signaling?
    Junhui Sun
    Systems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Free Radic Biol Med 54:105-12. 2013
    ..In conclusion, these results suggest that the protective effect of NO is not related primarily to activation of the sGC/cGMP/PKG signaling pathway, but rather through SNO signaling in IPC-induced acute cardioprotection...
  25. pmc Cysteine 203 of cyclophilin D is critical for cyclophilin D activation of the mitochondrial permeability transition pore
    Tiffany T Nguyen
    Systems Biology Center, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 286:40184-92. 2011
    ..Our results indicate that the Cys-203 residue of CypD is necessary for redox stress-induced activation of mPTP...
  26. ncbi request reprint Preconditioning: the mitochondrial connection
    Elizabeth Murphy
    National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Annu Rev Physiol 69:51-67. 2007
    ..This review focuses on mechanisms by which cardioprotection alters mitochondrial proteins and channels that regulate cell death and survival...
  27. ncbi request reprint Gender-based differences in mechanisms of protection in myocardial ischemia-reperfusion injury
    Elizabeth Murphy
    Vascular Medicine Branch, NHLBI, NIH, DHHS, Bethesda, MD 20892, USA
    Cardiovasc Res 75:478-86. 2007
    ..This review will summarize the data showing protection in females in animal studies and will summarize the data on possible mechanisms of cardioprotection in females...
  28. ncbi request reprint Cardioprotection in females: a role for nitric oxide and altered gene expression
    Elizabeth Murphy
    Head Cardiac Physiology Section, Vascular Medicine Branch, National Heart, Lung, and Blood Institute NIH, 10 Center Drive, Bethesda, MD 20892, USA
    Heart Fail Rev 12:293-300. 2007
    ..Taken together, estrogen by genomic and non-genomic pathways can result in the initiation of a number of signaling pathways that enhance cardioprotection...
  29. pmc Calcium-sensing receptor: a sensor and mediator of ischemic preconditioning in the heart
    Junhui Sun
    Translational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bldg 10 Rm 8N206, Bethesda, MD 20892, USA
    Am J Physiol Heart Circ Physiol 299:H1309-17. 2010
    ..Taken together, the distribution of CaSR in caveolae along with NPS2143-blockade of IPC-induced cardioprotective signaling suggest that the activation of CaSR during IPC is cardioprotective by a process involving caveolae...
  30. pmc Estrogen receptor activation and cardioprotection in ischemia reperfusion injury
    Anne M Deschamps
    National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Trends Cardiovasc Med 20:73-8. 2010
    ..In this review, we will focus on the signaling pathways leading to cardioprotection in ischemia reperfusion injury after ER activation and discuss the possibility and promise of specific ER modulators to treat ischemic heart diseases...
  31. pmc Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injury
    Hang Zhao
    Laboratory of Biochemistry, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 8012, USA
    Am J Physiol Heart Circ Physiol 301:H1513-8. 2011
    ..We conclude that cytosolic MsrA protects the heart from ischemia-reperfusion damage. The requirement for myristoylation suggests that MsrA must interact with a hydrophobic domain to provide protection...
  32. ncbi request reprint Protein kinase C and preconditioning: role of the sarcoplasmic reticulum
    Ken Yamamura
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T W Alexander Dr, Bldg 101, MD F2 07, Research Triangle Park, NC 27709, USA
    Am J Physiol Heart Circ Physiol 289:H2484-90. 2005
    ..These data suggest that activated PKC-epsilon reduces SR Ca2+ content through PLB dephosphorylation and that reduced SR Ca2+ may be important in cardioprotection...
  33. doi request reprint The NAD-dependent deacetylase SIRT2 is required for programmed necrosis
    Nisha Narayan
    Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, Maryland 20892, USA
    Nature 492:199-204. 2012
    ....
  34. pmc What makes the mitochondria a killer? Can we condition them to be less destructive?
    Elizabeth Murphy
    Translational Medicine Branch, NHLBI, NIH, Bethesda, MD 20892, USA
    Biochim Biophys Acta 1813:1302-8. 2011
    ..This article is part of a Special Issue entitled: Mitochondria and Cardioprotection...
  35. pmc Protein S-nitrosylation and cardioprotection
    Junhui Sun
    Translational Medicine Branch, NHLBI, NIH, 10 Center Dr, Room 7N112, Bethesda, MD 20892, USA
    Circ Res 106:285-96. 2010
    ..A better understanding of the mechanism regulating protein S-nitrosylation and its role in cardioprotection will provide us new therapeutic opportunities and targets for interventions in cardiovascular diseases...
  36. pmc Estrogen-enhanced gene expression of lipoprotein lipase in heart is antagonized by progesterone
    Dianxin Liu
    Laboratories of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA
    Endocrinology 149:711-6. 2008
    ..Progesterone also dose dependently inhibited the estrogen-mediated increase in LPL ERE reporter activity. These results show that heart LPL is an estrogen-responsive gene exhibiting an intronic regulatory sequence...
  37. pmc miR-222 contributes to sex-dimorphic cardiac eNOS expression via ets-1
    Alicia M Evangelista
    Systems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
    Physiol Genomics 45:493-8. 2013
    ..Our findings indicate that sex-dependent miR-222 regulation alters the expression of the cardiac regulatory protein eNOS...
  38. pmc S-nitrosylation: specificity, occupancy, and interaction with other post-translational modifications
    Alicia M Evangelista
    1 Systems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland
    Antioxid Redox Signal 19:1209-19. 2013
    ..SNO is a multifaceted post-translational modification, in that it can either act as a signaling molecule itself or as an intermediate to other modifications...
  39. ncbi request reprint Deoxymyoglobin is a nitrite reductase that generates nitric oxide and regulates mitochondrial respiration
    Sruti Shiva
    Vascular Medicine Branch, Clinical Center National Institutes of Health, Bethesda, MD 20892 1662, USA
    Circ Res 100:654-61. 2007
    ....
  40. ncbi request reprint Erythropoietin receptor expression in adult rat cardiomyocytes is associated with an acute cardioprotective effect for recombinant erythropoietin during ischemia-reperfusion injury
    Gary L Wright
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    FASEB J 18:1031-3. 2004
    ..These experiments revealed that the rapid cardioprotective effect of EPO during ischemia-reperfusion injury was associated with preservation of ATP levels in the ischemic myocardium...
  41. ncbi request reprint Bcl-2 regulation of mitochondrial energetics
    Elizabeth Murphy
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Trends Cardiovasc Med 15:283-90. 2005
    ..Understanding the physiologic processes controlled by Bcl-2 will be important in understanding cell regulation, and it may also provide new insights into the regulation of apoptosis...
  42. pmc What can we learn about cardioprotection from the cardiac mitochondrial proteome?
    Marjan Gucek
    NHLBI Proteomics Core, NHLBI, NIH, 10 Center Drive, Bethesda, MD 20892, USA
    Cardiovasc Res 88:211-8. 2010
    ..We focus on the cardiac mitochondrial proteome with emphasis on changes associated with cell death and protection, and we summarize how proteomic data have contributed to addressing the role of mitochondria in cardioprotection...
  43. pmc Mitochondrial permeability transition pore and calcium handling
    Renee Wong
    Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA
    Methods Mol Biol 810:235-42. 2012
    ..This chapter focuses on key issues in the study of the MPT and provides some methods for measuring MPT opening in isolated mitochondria...
  44. pmc The role of comorbidities in cardioprotection
    Michael N Sack
    Center for Molecular Medicine, NHLBI, NIH, Bethesda, MD, USA
    J Cardiovasc Pharmacol Ther 16:267-72. 2011
    ..It is important to understand at a mechanistic level the reasons for these differences. The effects of sex and diseases need to be considered in design of cardioprotective interventions in animal studies and clinical trials...
  45. ncbi request reprint Gender differences in sarcoplasmic reticulum calcium loading after isoproterenol
    Jarvis Chen
    Laboratories of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Am J Physiol Heart Circ Physiol 285:H2657-62. 2003
    ..Female myocytes also have significantly higher levels of neuronal NOS. This gender difference in SR Ca2+ handling may contribute to reduced ischemia-reperfusion injury observed in females...
  46. pmc Inhibit GSK-3beta or there's heartbreak dead ahead
    Elizabeth Murphy
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA
    J Clin Invest 113:1526-8. 2004
    ..The phosphorylation and inhibition of GSK-3beta lead to inhibition or delayed activation of the mitochondrial permeability transition, a key regulator of apoptosis...
  47. ncbi request reprint G protein-coupled receptor internalization signaling is required for cardioprotection in ischemic preconditioning
    Haiyan Tong
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Circ Res 94:1133-41. 2004
    ..We found that the catalytically inactive mutant of PI3Kgamma blocks the protection of PC. In summary, these data suggest the novel finding that the cardioprotective effect of PC requires receptor internalization...
  48. ncbi request reprint Inhibition of GSK-3beta as a target for cardioprotection: the importance of timing, location, duration and degree of inhibition
    Elizabeth Murphy
    National Institute of Environmental Health Sciences, Laboratory of Signal Transduction, NIH, DHHS, Research Triangle Park, NC 27709, USA
    Expert Opin Ther Targets 9:447-56. 2005
    ..Therapies for inhibiting GSK are feasible as there are a number of newly developed specific inhibitors of GSK available, although most of these drugs have not been tested in long-term animal studies...
  49. ncbi request reprint Acute hemorrhagic myocardial necrosis and sudden death of rats exposed to a combination of ephedrine and caffeine
    Abraham Nyska
    Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Toxicol Sci 83:388-96. 2005
    ..Our work shows the direct relationship between combined ephedrine and caffeine exposure and cardiac pathology...
  50. pmc S-nitrosylation: NO-related redox signaling to protect against oxidative stress
    Junhui Sun
    National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Antioxid Redox Signal 8:1693-705. 2006
    ..However, oxidative stress and the resultant dysfunction of NO signaling have been implicated in the pathogenesis of cardiovascular diseases...
  51. pmc Pivotal Role of mTORC2 and Involvement of Ribosomal Protein S6 in Cardioprotective Signaling
    Toshiyuki Yano
    From the Department of Pathology T Y, C S and Division of Cardiology, Department of Medicine M F, Johns Hopkins University, Baltimore, MD Proteomics Core A A and Systems Biology Center E M, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD and Departments of Cardiovascular, Renal, and Metabolic Medicine T Y, A K, T M and Pharmacology A K, Sapporo Medical University, Sapporo, Japan
    Circ Res 114:1268-80. 2014
    ..There is tight coupling between Akt activation and suppression of cell death. Full Akt activation requires mammalian target of rapamycin complex 2 (mTORC2), but the regulation of mTORC2 is unclear...
  52. pmc S-nitrosylation of TRIM72 at cysteine 144 is critical for protection against oxidation-induced protein degradation and cell death
    Mark J Kohr
    Systems Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA Division of Cardiovascular Pathology, Department of Pathology, 720 Rutland Avenue, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA Electronic address
    J Mol Cell Cardiol 69:67-74. 2014
    ....
  53. pmc Does the voltage dependent anion channel modulate cardiac ischemia-reperfusion injury?
    Samarjit Das
    Department of Pathology, Johns Hopkins Medical Institute and Systems Biology Center, NHLBI, NIH, Bethesda, MD, USA
    Biochim Biophys Acta 1818:1451-6. 2012
    ..This article is part of a Special Issue entitled: VDAC structure, function, and regulation of mitochondrial metabolism...
  54. ncbi request reprint Is Na/Ca exchange during ischemia and reperfusion beneficial or detrimental?
    Elizabeth Murphy
    Laboratory of Signal Transduction, National Institute for Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Ann N Y Acad Sci 976:421-30. 2002
    ..These studies suggest that overexpression of the Na/Ca exchanger enhances injury in males, but females are protected by a gender-related mechanism...
  55. ncbi request reprint Treatment with an estrogen receptor-beta-selective agonist is cardioprotective
    Ivana Nikolic
    Laboratory of Signal Transduction, NIEHS, NIH, DHHS, Durham, NC, USA
    J Mol Cell Cardiol 42:769-80. 2007
    ..Gene profiling showed that treatment with DPN resulted in upregulation of a number of protective genes such as heat shock protein 70, the antiapoptotic protein, growth arrest and DNA damage 45 beta, and cyclooxygenase 2...
  56. ncbi request reprint Ephedrine plus caffeine causes age-dependent cardiovascular responses in Fischer 344 rats
    Reuben Howden
    Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Am J Physiol Heart Circ Physiol 288:H2219-24. 2005
    ..The greater mortality in the 14-wk-old rats was associated with increases in body temperature, HR, and myocardial necrosis...
  57. pmc Transient upregulation of PGC-1alpha diminishes cardiac ischemia tolerance via upregulation of ANT1
    Edward G Lynn
    Translational Medicine Branch, NHLBI, NIH, Bethesda, MD 20892 1454, USA
    J Mol Cell Cardiol 49:693-8. 2010
    ..These adverse phenotypes appear to be mediated, in part, by PGC-1alpha induced upregulation of ANT1...
  58. ncbi request reprint Primary and secondary signaling pathways in early preconditioning that converge on the mitochondria to produce cardioprotection
    Elizabeth Murphy
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, US Department of Health and Human Services, Research Triangle Park, NC, USA
    Circ Res 94:7-16. 2004
    ..Alterations in these mitochondrial proteins results in altered metabolism and inhibition of cell death, thus resulting in cardioprotection...
  59. ncbi request reprint Activation of the prolyl hydroxylase oxygen-sensor results in induction of GLUT1, heme oxygenase-1, and nitric-oxide synthase proteins and confers protection from metabolic inhibition to cardiomyocytes
    Gary Wright
    Laboratory of Signal Transduction, Department of Health and Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 278:20235-9. 2003
    ..These results point to a key role for the PHD pathway in the phenotypic changes that are observed in a hypoxic myocyte and may suggest a strategy to pharmacologically induce protection in heart...
  60. ncbi request reprint Enhanced postischemic functional recovery in CYP2J2 transgenic hearts involves mitochondrial ATP-sensitive K+ channels and p42/p44 MAPK pathway
    John Seubert
    Division of Intramural Research, NIEHS NIH, Research Triangle Park, NC 27709, USA
    Circ Res 95:506-14. 2004
    ..Together, these data suggest that CYP2J2-derived metabolites are cardioprotective after ischemia, and the mechanism for this cardioprotection involves activation of mitoK(ATP) and p42/p44 MAPK...
  61. ncbi request reprint Phosphorylation of glycogen synthase kinase-3beta during preconditioning through a phosphatidylinositol-3-kinase--dependent pathway is cardioprotective
    Haiyan Tong
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Circ Res 90:377-9. 2002
    ..These findings indicate that inhibition of GSK-3beta is protective and that this PI3-kinase--dependent signaling pathway may play an important role in ischemic preconditioning...
  62. ncbi request reprint Inhibition of delta-protein kinase C protects against reperfusion injury of the ischemic heart in vivo
    Koichi Inagaki
    Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, Calif 94305 5174, USA
    Circulation 108:2304-7. 2003
    ..We focus here on the role for deltaPKC during reperfusion only, using an in vivo porcine model of AMI...
  63. ncbi request reprint Expression of activated PKC epsilon (PKC epsilon) protects the ischemic heart, without attenuating ischemic H(+) production
    Heather R Cross
    Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    J Mol Cell Cardiol 34:361-7. 2002
    ..Protection occurred in the PKC epsilon hearts without attenuation of ischemic H(+) production, implying that, at least in this ischemic model, reduced acidification during ischemia is not necessary for cardioprotection...
  64. ncbi request reprint Ablation of PLB exacerbates ischemic injury to a lesser extent in female than male mice: protective role of NO
    Heather R Cross
    Department of Pathology, Duke University Medical Center, Durham 27710, USA
    Am J Physiol Heart Circ Physiol 284:H683-90. 2003
    ..Protection in females was decreased by a NOS inhibitor and mimicked in males by an NO donor, implying that protection was NOS mediated...
  65. ncbi request reprint Ca(2+) loading and adrenergic stimulation reveal male/female differences in susceptibility to ischemia-reperfusion injury
    Heather R Cross
    Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Am J Physiol Heart Circ Physiol 283:H481-9. 2002
    ..Females were therefore protected from the detrimental effects of adrenergic stimulation and Ca(2+) loading via a NOS-mediated mechanism...
  66. pmc Overexpression of A(3) adenosine receptors decreases heart rate, preserves energetics, and protects ischemic hearts
    Heather R Cross
    Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Am J Physiol Heart Circ Physiol 283:H1562-8. 2002
    ..Therefore, A(3)AR overexpression results in cardioprotection via a specific A(3)AR effect, possibly involving preservation of ATP during ischemia...
  67. ncbi request reprint Male and female mice overexpressing the beta(2)-adrenergic receptor exhibit differences in ischemia/reperfusion injury: role of nitric oxide
    Heather R Cross
    Department of Pathology, Box 3712, Duke University Medical Center, Durham, NC 27710, USA
    Cardiovasc Res 53:662-71. 2002
    ....
  68. pmc Role of soluble epoxide hydrolase in postischemic recovery of heart contractile function
    John M Seubert
    Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada
    Circ Res 99:442-50. 2006
    ..Together, these data suggest that targeted disruption of sEH increases the availability of cardioprotective EETs that work by activating PI3K signaling pathways and K+ channels...
  69. ncbi request reprint Hypercontractile female hearts exhibit increased S-nitrosylation of the L-type Ca2+ channel alpha1 subunit and reduced ischemia/reperfusion injury
    Junhui Sun
    National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Circ Res 98:403-11. 2006
    ....
  70. ncbi request reprint The nuclear receptor ERRalpha is required for the bioenergetic and functional adaptation to cardiac pressure overload
    Janice M Huss
    Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Metab 6:25-37. 2007
    ..These results demonstrate that the nuclear receptor ERRalpha is required for the adaptive bioenergetic response to hemodynamic stressors known to cause heart failure...
  71. pmc Mitochondrial dysfunction and apoptosis underlie the pathogenic process in alpha-B-crystallin desmin-related cardiomyopathy
    Alina Maloyan
    Division of Molecular Cardiovascular Biology, Cincinnati Children s Hospital, Cincinnati, Ohio, USA
    Circulation 112:3451-61. 2005
    ....
  72. ncbi request reprint Cardiac-specific ablation of the Na+-Ca2+ exchanger confers protection against ischemia/reperfusion injury
    Kenichi Imahashi
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Circ Res 97:916-21. 2005
    ..Thus, NCX-KO hearts were significantly protected against ischemia-reperfusion injury, suggesting that Ca2+ entry via reverse-mode NCX is a major cause of ischemia/reperfusion injury...
  73. pmc Glycogen synthase kinase 3 inhibition slows mitochondrial adenine nucleotide transport and regulates voltage-dependent anion channel phosphorylation
    Samarjit Das
    Department of Pathology, Johns Hopkins University, Baltimore, MD 21205, USA
    Circ Res 103:983-91. 2008
    ..Both proteomics and adenine nucleotide transport data suggest that GSK regulates VDAC and that VDAC may be an important regulatory site in ischemia/reperfusion injury...
  74. ncbi request reprint The role of beta-adrenergic receptor signaling in cardioprotection
    Haiyan Tong
    Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
    FASEB J 19:983-5. 2005
    ..These data show an important role for beta2-AR in cardioprotection and support the novel hypothesis that preconditioning involves switching of beta2-AR coupling from Gs to Gi...
  75. ncbi request reprint A practical guide for clinicians who treat patients with amiodarone: 2007
    Nora Goldschlager
    University of California, San Francisco, California, USA
    Heart Rhythm 4:1250-9. 2007
    ..The recommendations included herein are based on the best available data and the collective experience of the member of the writing committee...
  76. ncbi request reprint Targeted deletion of thioredoxin-interacting protein regulates cardiac dysfunction in response to pressure overload
    Jun Yoshioka
    Cardiovascular Division, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    Circ Res 101:1328-38. 2007
    ..These results support the emerging concept that the function of Txnip is not as a simple thioredoxin inhibitor but as a metabolic control protein...
  77. pmc Detection of human CYP2C8, CYP2C9, and CYP2J2 in cardiovascular tissues
    Tracy C DeLozier
    National Institute of Environmental Health Sciences, 111 T W Alexander Drive, Research Triangle Park, NC 27709, USA
    Drug Metab Dispos 35:682-8. 2007
    ..The expression of CYP2J2 and CYP2C8 in human heart, and CYPC9 and CYP2J2 in aorta and coronary artery is consistent with a physiological role for these enzymes in these tissues...
  78. ncbi request reprint Estrogen receptor-beta mediates male-female differences in the development of pressure overload hypertrophy
    Maryanne Skavdahl
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Am J Physiol Heart Circ Physiol 288:H469-76. 2005
    ..These data suggest an important role for estrogen receptor-beta in attenuating the hypertrophic response to pressure overload in females...
  79. ncbi request reprint How does endothelin-1 cause a sustained increase in intracellular sodium and calcium which lead to hypertrophy?
    Elizabeth Murphy
    J Mol Cell Cardiol 41:782-4. 2006
  80. ncbi request reprint Alterations in apoptotic signaling in human idiopathic cardiomyopathic hearts in failure
    Charles Steenbergen
    Department of Pathology, Duke University Medical Center, Durham 27710, USA
    Am J Physiol Heart Circ Physiol 284:H268-76. 2003
    ..This study identifies several pathways that are altered in human heart failure and provides new targets for therapy...
  81. ncbi request reprint Preconditioning: is the Akt-ion in the PI3K pathway?
    Elizabeth Murphy
    J Mol Cell Cardiol 35:1021-5. 2003
  82. ncbi request reprint Mechanisms of erythropoietin-mediated cardioprotection during ischemia-reperfusion injury: role of protein kinase C and phosphatidylinositol 3-kinase signaling
    Paul R Hanlon
    Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
    FASEB J 19:1323-5. 2005
    ..Postischemia cardioprotection by EPO required the PI3K pathway but was not affected by inhibition of PKC at the time of EPO treatment...
  83. ncbi request reprint Nuclear targeting of Akt enhances kinase activity and survival of cardiomyocytes
    Isao Shiraishi
    The Children s Hospital Research Foundation, Division of Molecular Cardiovascular Biology Cincinnati, Ohio, USA
    Circ Res 94:884-91. 2004
    ....
  84. ncbi request reprint Estrogen receptor beta mediates gender differences in ischemia/reperfusion injury
    Scott A Gabel
    Laboratories of Structural Biology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    J Mol Cell Cardiol 38:289-97. 2005
    ..We further showed that WT female hearts have increased ratio of carbohydrate to fatty acid metabolism relative to WT males...
  85. pmc Signalosomes: delivering cardioprotective signals from GPCRs to mitochondria
    Elizabeth Murphy
    Am J Physiol Heart Circ Physiol 295:H920-H922. 2008