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Genomes and Genes | Elizabeth MurphySummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
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...- Mechanisms underlying acute protection from cardiac ischemia-reperfusion injuryElizabeth 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... - Ion transport and energetics during cell death and protectionElizabeth 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... - 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 - Regulation of intracellular and mitochondrial sodium in health and diseaseElizabeth 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... - Estrogen signaling and cardiovascular diseaseElizabeth 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... - Sex differences in the phosphorylation of mitochondrial proteins result in reduced production of reactive oxygen species and cardioprotection in femalesClaudia 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... - Disruption of caveolae blocks ischemic preconditioning-mediated S-nitrosylation of mitochondrial proteinsJunhui 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... - Cardioprotection leads to novel changes in the mitochondrial proteomeRenee 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... - Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female ratsAnne 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... - Measurement of S-nitrosylation occupancy in the myocardium with cysteine-reactive tandem mass tags: short communicationMark 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... 
Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transportJunhui 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...- Male/female differences in intracellular Na+ regulation during ischemia/reperfusion in mouse heartKenichi 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... - Transgenic expression of Bcl-2 modulates energy metabolism, prevents cytosolic acidification during ischemia, and reduces ischemia/reperfusion injuryKenichi 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... - Acute inhibition of GSK causes mitochondrial remodelingTiffany 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... - S-nitrosylation: a radical way to protect the heartElizabeth 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.".. - Overexpression of the Na+/H+ exchanger and ischemia-reperfusion injury in the myocardiumKenichi 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... - Cysteine 203 of cyclophilin D is critical for cyclophilin D activation of the mitochondrial permeability transition poreTiffany 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... - Protein kinase C and preconditioning: role of the sarcoplasmic reticulumKen 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... - Cardioprotection in females: a role for nitric oxide and altered gene expressionElizabeth 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... - Calcium-sensing receptor: a sensor and mediator of ischemic preconditioning in the heartJunhui 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... - Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injuryHang 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... - Gender-based differences in mechanisms of protection in myocardial ischemia-reperfusion injuryElizabeth 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... - Preconditioning: the mitochondrial connectionElizabeth 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... - Estrogen receptor activation and cardioprotection in ischemia reperfusion injuryAnne 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... - Estrogen-enhanced gene expression of lipoprotein lipase in heart is antagonized by progesteroneDianxin 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... - 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... - Protein S-nitrosylation and cardioprotectionJunhui 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... - Deoxymyoglobin is a nitrite reductase that generates nitric oxide and regulates mitochondrial respirationSruti Shiva
Vascular Medicine Branch, Clinical Center National Institutes of Health, Bethesda, MD 20892 1662, USA
Circ Res 100:654-61. 2007.... - 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... - Bcl-2 regulation of mitochondrial energeticsElizabeth 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... - Erythropoietin receptor expression in adult rat cardiomyocytes is associated with an acute cardioprotective effect for recombinant erythropoietin during ischemia-reperfusion injuryGary 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... - CypD(-/-) hearts have altered levels of proteins involved in Krebs cycle, branch chain amino acid degradation and pyruvate metabolismSara 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... - 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... - Mitochondrial permeability transition pore and calcium handlingRenee 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... - The role of comorbidities in cardioprotectionMichael 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... - Gender differences in sarcoplasmic reticulum calcium loading after isoproterenolJarvis 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... - Inhibition of GSK-3beta as a target for cardioprotection: the importance of timing, location, duration and degree of inhibitionElizabeth 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... - G protein-coupled receptor internalization signaling is required for cardioprotection in ischemic preconditioningHaiyan 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... - Inhibit GSK-3beta or there's heartbreak dead aheadElizabeth 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... - Acute hemorrhagic myocardial necrosis and sudden death of rats exposed to a combination of ephedrine and caffeineAbraham 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... - S-nitrosylation: NO-related redox signaling to protect against oxidative stressJunhui 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... - Treatment with an estrogen receptor-beta-selective agonist is cardioprotectiveIvana 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... - 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... - Ephedrine plus caffeine causes age-dependent cardiovascular responses in Fischer 344 ratsReuben 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... - Primary and secondary signaling pathways in early preconditioning that converge on the mitochondria to produce cardioprotectionElizabeth 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... - Transient upregulation of PGC-1alpha diminishes cardiac ischemia tolerance via upregulation of ANT1Edward 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... - 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... - 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 cardiomyocytesGary 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... - Enhanced postischemic functional recovery in CYP2J2 transgenic hearts involves mitochondrial ATP-sensitive K+ channels and p42/p44 MAPK pathwayJohn 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... - Expression of activated PKC epsilon (PKC epsilon) protects the ischemic heart, without attenuating ischemic H(+) productionHeather 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... - Ca(2+) loading and adrenergic stimulation reveal male/female differences in susceptibility to ischemia-reperfusion injuryHeather 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... - Overexpression of A(3) adenosine receptors decreases heart rate, preserves energetics, and protects ischemic heartsHeather 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... - Ablation of PLB exacerbates ischemic injury to a lesser extent in female than male mice: protective role of NOHeather 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... - Inhibition of delta-protein kinase C protects against reperfusion injury of the ischemic heart in vivoKoichi Inagaki
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, Calif 94305-5174, USA
Circulation 108:2304-7. 2003..CONCLUSIONS: Reperfusion injury after cardiac ischemia is mediated, at least in part, by deltaPKC activation. This study suggests that including a deltaPKC inhibitor at reperfusion may improve the outcome for patients with AMI... - Cardiac-specific ablation of the Na+-Ca2+ exchanger confers protection against ischemia/reperfusion injuryKenichi 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... - Phosphorylation of glycogen synthase kinase-3beta during preconditioning through a phosphatidylinositol-3-kinase--dependent pathway is cardioprotectiveHaiyan 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... - Male and female mice overexpressing the beta(2)-adrenergic receptor exhibit differences in ischemia/reperfusion injury: role of nitric oxideHeather R Cross
Department of Pathology, Box 3712, Duke University Medical Center, Durham, NC 27710, USA
Cardiovasc Res 53:662-71. 2002.... - Mitochondrial dysfunction and apoptosis underlie the pathogenic process in alpha-B-crystallin desmin-related cardiomyopathyAlina Maloyan
Division of Molecular Cardiovascular Biology, Cincinnati Children s Hospital, Cincinnati, Ohio, USA
Circulation 112:3451-61. 2005.... - The role of beta-adrenergic receptor signaling in cardioprotectionHaiyan 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... - The nuclear receptor ERRalpha is required for the bioenergetic and functional adaptation to cardiac pressure overloadJanice 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... - Glycogen synthase kinase 3 inhibition slows mitochondrial adenine nucleotide transport and regulates voltage-dependent anion channel phosphorylationSamarjit 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... - Hypercontractile female hearts exhibit increased S-nitrosylation of the L-type Ca2+ channel alpha1 subunit and reduced ischemia/reperfusion injuryJunhui Sun
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Circ Res 98:403-11. 2006.... - Role of soluble epoxide hydrolase in postischemic recovery of heart contractile functionJohn 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... - A practical guide for clinicians who treat patients with amiodarone: 2007Nora 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... - Alterations in apoptotic signaling in human idiopathic cardiomyopathic hearts in failureCharles 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... - Targeted deletion of thioredoxin-interacting protein regulates cardiac dysfunction in response to pressure overloadJun 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... - Detection of human CYP2C8, CYP2C9, and CYP2J2 in cardiovascular tissuesTracy 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... - Mechanisms of erythropoietin-mediated cardioprotection during ischemia-reperfusion injury: role of protein kinase C and phosphatidylinositol 3-kinase signalingPaul 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... - Preconditioning: is the Akt-ion in the PI3K pathway?Elizabeth Murphy
J Mol Cell Cardiol 35:1021-5. 2003 - Signalosomes: delivering cardioprotective signals from GPCRs to mitochondriaElizabeth Murphy
Am J Physiol Heart Circ Physiol 295:H920-H922. 2008 - Nuclear targeting of Akt enhances kinase activity and survival of cardiomyocytesIsao Shiraishi
The Children s Hospital Research Foundation, Division of Molecular Cardiovascular Biology Cincinnati, Ohio, USA
Circ Res 94:884-91. 2004.... - Estrogen receptor beta mediates gender differences in ischemia/reperfusion injuryScott 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... - Estrogen receptor-beta mediates male-female differences in the development of pressure overload hypertrophyMaryanne 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... - 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