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Search Results to Mahesh P. Gupta

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One or more keywords matched the following properties of Gupta, Mahesh P.

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 Sirtuins
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 SIRT3 is a stress-responsive deacetylase in cardiomyocytes that protects cells from stress-mediated cell death by deacetylation of Ku70.
Academic Article SIRT1 promotes cell survival under stress by deacetylation-dependent deactivation of poly(ADP-ribose) polymerase 1.
Academic Article Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice.
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 SIRT6 promotes COX-2 expression and acts as an oncogene in skin cancer.
Academic Article Posttranslational modification of Sirt6 activity by peroxynitrite.
Academic Article Regulation of Akt signaling by sirtuins: its implication in cardiac hypertrophy and aging.
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 Cellular mechanisms promoting cachexia and how they are opposed by sirtuins 1.
Academic Article The histone deacetylase SIRT6 blocks myostatin expression and development of muscle atrophy.
Grant Activation of sirtuins to prevent adverse cardiac remodeling after CABG
Grant Exploring roles of sirtuins in protecting diabetic hearts
Grant Blocking cardiac toxicity of anticancer drugs
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 Is nuclear sirtuin SIRT6 a master regulator of immune function?
Academic Article The nuclear sirtuin SIRT6 protects the heart from developing aging-associated myocyte senescence and cardiac hypertrophy.

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  • Sirtuins