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10.1155/2018/7293861 http://scihub22266oqcxt.onion/10.1155/2018/7293861 C5831850!5831850!29643974     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29643974&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Oxid+Med+Cell+Longev 2018 ; 2018 (ä): ä Nephropedia Template TP {{tp|p=29643974|t=2018. SIRT3: A New Regulator of Cardiovascular Diseases |pdf=|usr=}}{{29643974}} gab.com Text SIRT3: A New Regulator of Cardiovascular Diseases JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=29643974 #FOAvip Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and defects in mitochondrial function contribute largely to the occurrence of CVDs. Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD+-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation. SIRT3 regulates glucose and lipid metabolism and maintains myocardial ATP levels, which protects the heart from metabolic disturbances. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy. Recent reports show that SIRT3 is involved in the protection of several heart diseases. This review discusses the progress in SIRT3-related research and the role of SIRT3 in the prevention and treatment of CVDs. Twit Text FOAVip SIRT3: A New Regulator of Cardiovascular Diseases ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=29643974 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29643974 #FOAvip English Wikipedia <ref>{{Cite pmid|29643974}}</ref> SIRT3: A New Regulator of Cardiovascular Diseases #MMPMID29643974 Sun W; Liu C; Chen Q; Liu N; Yan Y; Liu B Oxid Med Cell Longev 2018[]; 2018 (ä): ä PMID29643974show ga Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and defects in mitochondrial function contribute largely to the occurrence of CVDs. Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD+-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation. SIRT3 regulates glucose and lipid metabolism and maintains myocardial ATP levels, which protects the heart from metabolic disturbances. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy. Recent reports show that SIRT3 is involved in the protection of several heart diseases. This review discusses the progress in SIRT3-related research and the role of SIRT3 in the prevention and treatment of CVDs. äSIRT3: A New Regulator of Cardiovascular Diseases (epmc).pdf DeepDyve Pubget Overpricing