Cardiovascular disease (CVD) is currently a major factor affecting human physical and mental health. In recent years, the relationship between intracellular Ca and CVD has been extensively studied. Ca movement across the mitochondrial inner membrane plays a vital role as an intracellular messenger, regulating energy metabolism and calcium homeostasis. It is also involved in pathological processes such as cardiomyocyte apoptosis, hypertrophy and fibrosis in CVD. The selective mitochondrial calcium uniporter complex (MCU complex) located in the inner membrane is essential for mitochondrial Ca uptake. Therefore, the MCU complex is a potential therapeutic target for CVD. In this review, recent research progress on the pathophysiological mechanisms and therapeutic potential of the MCU complex in various CVDs was summarized, including myocardial ischemia‑reperfusion injury, pulmonary arterial hypertension, other peripheral vascular diseases, myocardial remodeling and arrhythmias. This review contributes to a deeper understanding of these mechanisms at the molecular level and highlights potential intervention targets for CVD treatment in clinical practice.
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http://dx.doi.org/10.3892/ijmm.2024.5481 | DOI Listing |
Int J Mol Med
March 2025
Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan 421000, P.R. China.
Cardiovascular disease (CVD) is currently a major factor affecting human physical and mental health. In recent years, the relationship between intracellular Ca and CVD has been extensively studied. Ca movement across the mitochondrial inner membrane plays a vital role as an intracellular messenger, regulating energy metabolism and calcium homeostasis.
View Article and Find Full Text PDFEMBO Rep
December 2024
Molecular Physiology, Institute of Cardiovascular Physiology, University Medical Centre, Georg-August-University, Göttingen, Germany.
J Appl Physiol (1985)
January 2025
Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Chofu, Tokyo, Japan.
Eccentric contractions (ECC) are accompanied by the accumulation of intracellular calcium ions ([Ca]) and induce skeletal muscle damage. Suppressed muscle damage in repeated bouts of ECC is well characterized; however, whether it is mediated by altered Ca profiles remains unknown. We tested the hypothesis that repeated ECC suppresses Ca accumulation via adaptations in Ca regulation.
View Article and Find Full Text PDFPLoS Biol
November 2024
Laboratory of Calciomics and Systemic Pathophysiology (LCSP), Regional Centre for Biotechnology (RCB), Faridabad, Delhi-NCR, India.
Mitochondria regulate several physiological functions through mitochondrial Ca2+ dynamics. However, role of mitochondrial Ca2+ signaling in melanosome biology remains unknown. Here, we show that pigmentation requires mitochondrial Ca2+ uptake.
View Article and Find Full Text PDFSci China Life Sci
October 2024
Shanghai Institute of Medical Genetics, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200040, China.
Autosomal recessive spinocerebellar ataxias (SCARs) are one of the most common neurodegenerative diseases characterized by progressive ataxia. Although SCARs are known to be caused by mutations in multiple genes, there are still many cases that go undiagnosed or are misdiagnosed. In this study, we presented a SCAR patient, and identified a probable novel pathogenic mutation (c.
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