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One or more keywords matched the following properties of Gupta, Mahesh P.
PropertyValue
keywords Heart Failure, cardiac aging, Sirtuins, diabetes, mitochondria, Sepsis, Cachexia
overview Primary focus of my lab is to understand the molecular basis of heart failure, particularly, the role played by the chromatin remodeling enzymes in muscle gene regulation, cellular senescence and cardiac hypertrophy and fibrosis. Heart failure is a pathological state in which the heart is unable to pump blood at a rate commensurate with requirements of the metabolizing tissues. It is usually caused by a defect in myocardial contraction. Reduced myocardial contractile function may reflect a decrease in number of viable myocytes, dysfunction of viable myocytes, or alterations to the intrinsic contractile activity of individual myocytes. At the molecular level, several abnormalities have been observed, including alterations in the expression of numerous genes that are central to the normal structure and function of the heart; however, the basic mechanism of heart failure is not yet fully understood. With recent advancements in cell biology, it has become clear that factors modifying chromatin structure, e.g. histone deacetylases, acetyltransferases and sirtuins play a fundamental role in this process. In addition to modifying chromatin structure, these enzymes also play a role out side the nucleus. We are trying to understand how these enzymes modify mitochondrial proteins and regulate the cell-survivability and contractile function, in response to various pathophysiological stresses, including obesity/diabetes, hemodynamic overloads and aging.
One or more keywords matched the following items that are connected to Gupta, Mahesh P.
Item TypeName
Concept Heart
Concept Heart Diseases
Concept Heart Failure
Concept Heart Ventricles
Concept Mitochondria, Heart
Concept Heart Valve Prosthesis Implantation
Academic Article Increased expression of alternatively spliced dominant-negative isoform of SRF in human failing hearts.
Academic Article Single-stranded DNA-binding proteins PURalpha and PURbeta bind to a purine-rich negative regulatory element of the alpha-myosin heavy chain gene and control transcriptional and translational regulation of the gene expression. Implications in the repression of alpha-myosin heavy chain during heart failure.
Academic Article Increased expression of poly(ADP-ribose) polymerase-1 contributes to caspase-independent myocyte cell death during heart failure.
Academic Article Poly(ADP-ribose) polymerase-1-dependent cardiac myocyte cell death during heart failure is mediated by NAD+ depletion and reduced Sir2alpha deacetylase activity.
Academic Article Poly(ADP-ribose) polymerase-1-deficient mice are protected from angiotensin II-induced cardiac hypertrophy.
Academic Article Concurrent opposite effects of trichostatin A, an inhibitor of histone deacetylases, on expression of alpha-MHC and cardiac tubulins: implication for gain in cardiac muscle contractility.
Academic Article Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure.
Academic Article Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro.
Academic Article A novel cardiomyocyte-enriched microRNA, miR-378, targets insulin-like growth factor 1 receptor: implications in postnatal cardiac remodeling and cell survival.
Academic Article Mitochondrial SIRT3 and heart disease.
Academic Article The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun.
Academic Article Activation of SIRT1, a class III histone deacetylase, contributes to fructose feeding-mediated induction of the alpha-myosin heavy chain expression.
Academic Article Exogenous NAD blocks cardiac hypertrophic response via activation of the SIRT3-LKB1-AMP-activated kinase pathway.
Academic Article Emerging roles of SIRT1 deacetylase in regulating cardiomyocyte survival and hypertrophy.
Academic Article Nampt secreted from cardiomyocytes promotes development of cardiac hypertrophy and adverse ventricular remodeling.
Academic Article SIRT3 deacetylates and activates OPA1 to regulate mitochondrial dynamics during stress.
Academic Article Obesity-induced lysine acetylation increases cardiac fatty acid oxidation and impairs insulin signalling.
Academic Article In situ constructive myocardial remodeling of extracellular matrix patch enhanced with controlled growth factor release.
Academic Article Sirt3 protects mitochondrial DNA damage and blocks the development of doxorubicin-induced cardiomyopathy in mice.
Academic Article Role of Sirtuins in Regulating Pathophysiology of the Heart.
Academic Article Honokiol, an activator of Sirtuin-3 (SIRT3) preserves mitochondria and protects the heart from doxorubicin-induced cardiomyopathy in mice.
Academic Article Molecular regulation of mitochondrial dynamics in cardiac disease.
Award or Honor Receipt Senior Reserach Fellowship
Award or Honor Receipt Fellow of American Heart Association (FAHA)
Award or Honor Receipt Upjohn Award for the best research paper
Grant Histone deacetylases in pathogenesis of heart failure
Grant Activation of sirtuins to prevent adverse cardiac remodeling after CABG
Grant Improving post-surgery recovery of failing hearts by targeting cardiomyocyte senescence
Grant The Role of PARP-SIR2 Signaling in Heart Failure
Grant Exploring roles of sirtuins in protecting diabetic hearts
Grant Blocking cardiac toxicity of anticancer drugs
Grant Alpha-Myosin Heavy Chain Gene Repression &Heart Failure
Academic Article The nuclear and mitochondrial sirtuins, Sirt6 and Sirt3, regulate each other's activity and protect the heart from developing obesity-mediated diabetic cardiomyopathy.
Academic Article The nuclear sirtuin SIRT6 protects the heart from developing aging-associated myocyte senescence and cardiac hypertrophy.
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  • Heart