Mitochondria represent the heart unit of the cardiac cell because they are involved in ATP production and in the transfer to the contractile apparatus. Furthermore, mitochondria modulate Ca2+ homeostasis, manage redox status, and regulate response to cellular and environmental stresses. Abnormalities in mitochondrial organelle structure and function have been observed in many cardiovascular diseases, such as ischemic cardiomyopathy, heart failure, and stroke, and in drug-induced cardiomyopathies. This review summarizes the recent literature in this field.
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http://dx.doi.org/10.1615/CritRevEukaryotGeneExpr.2019028579 | DOI Listing |
Free Radic Biol Med
January 2025
Department of Radiation Oncology, Mays Cancer Center at UT Health San Antonio MD Anderson, Joe R. and Teresa Lozano Long School of Medicine, TX, USA. Electronic address:
Manganese superoxide dismutase (MnSOD/SOD2) is an essential mitochondrial enzyme that detoxifies superoxide radicals generated during oxidative respiration. MnSOD/SOD2 lysine 68 acetylation (K68-Ac) is an important post-translational modification (PTM) that regulates enzymatic activity, responding to nutrient status or oxidative stress, and elevated levels have been associated with human illness. To determine the in vivo role of MnSOD-K68 in the heart, we used a whole-body non-acetylation mimic mutant (MnSOD) knock-in mouse.
View Article and Find Full Text PDFJACC Basic Transl Sci
December 2024
Vascular Metabolism Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
Exercise intolerance, a hallmark of heart failure with preserved ejection fraction (HFpEF) exacerbated by obesity, involves unclear mechanisms related to skeletal muscle metabolism. In a "2-hit" model of HFpEF, we investigated the ability of exercise therapy (voluntary wheel running) to reverse skeletal muscle dysfunction and exercise intolerance. Using state-of-the-art metabolic cages and a multiomic approach, we demonstrate exercise can rescue dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restore exercise capacity in mice with cardiometabolic HFpEF.
View Article and Find Full Text PDFJACC Basic Transl Sci
December 2024
Department of Cardiovascular Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Front Med
January 2025
Department of Pharmacology (SKLFZCD, State Key Laboratory-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin, 150081, China.
Diabetic cardiomyopathy (DCM) is a medical condition characterized by cardiac remodeling and dysfunction in individuals with diabetes mellitus. Sarcoplasmic reticulum (SR) and mitochondrial Ca overload in cardiomyocytes have been recognized as biological hallmarks in DCM; however, the specific factors underlying these abnormalities remain largely unknown. In this study, we aimed to investigate the role of a cardiac-specific long noncoding RNA, D830005E20Rik (Trdn-as), in DCM.
View Article and Find Full Text PDFExp Cell Res
January 2025
Cardiovascular Center, College of Medicine, University of Cincinnati, Ohio-45267, United States of America; School of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur-613401, Tamil Nadu, India. Electronic address:
Multiple forms of cell death contribute significantly to cardiovascular pathologies, negatively impacting cardiac remodeling and leading to heart failure. While myocardial cell death has been associated with PM induced cardiotoxicity, the temporal dynamics of various cell death forms, such as apoptosis, ferroptosis, necroptosis, and pyroptosis, in relation to inflammatory processes, remain underexplored. This study examines the time-dependent onset and progression of these cell death pathways in the myocardium and their correlation with inflammation in a Wistar rat model.
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