Why the study?
Impaired sarcoplasmic reticulum-mitochondrial calcium communication may contribute to cardiovascular disease progression, representing a potential therapeutic target.
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Design
Review
SR-mitochondrial calcium dysregulation may represent a CVD therapeutic target; leaves open the need for prospective trials before clinical adoption.
Cardiovascular disease (CVD) remains a leading cause of mortality and disability globally. Various cardiovascular diseases are often associated with ion dyshomeostasis within and outside cardiomyocytes, such as sodium ions, calcium ions and potassium ions. Calcium ions (Ca 2 + ) not only participate in the contractile activity of cardiomyocytes and smooth muscle cells, but also participate in the tricarboxylic acid cycle as a cellular energy source, and act as a second messengers during many biological processes. Consequently, the concentration of calcium ions inside and outside the cell, as well as the distribution of calcium ions in various organelles and the cytoplasm are critical. Sarcoplasmic reticulum (SR)-mitochondrial calcium communication plays a crucial role in the distribution of Ca 2+ in the cytoplasm and organelles. Disturbed calcium signaling caused by impaired calcium communication between the sarcoplasmic reticulum and mitochondria may play a significant role in the pathogenesis of cardiovascular diseases. Recent studies have increasingly demonstrated the significant role of SR-mitochondrial calcium communication in the progression of cardiovascular diseases, suggesting its potential as a therapeutic target. This review provides a summary of existing evidence supporting the contribution of SR-mitochondrial calcium communication disorders to the development of CVD, emphasizing its potential as a promising therapeutic target for CVD management.
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Wang et al. (2025) studied this question.
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