Why the study?
Chronic heart failure carries a poor prognosis and high mortality, and recent evidence indicates aging and cellular senescence play vital roles in its development.
Cellular senescence and related mechanisms play a vital role in chronic heart failure pathogenesis, presenting potential novel therapeutic targets.
Senescence pathways in CHF merit targeted research; leaves open clinical translation or therapies.
Chronic heart failure (CHF) is the final stage of heart disease and is caused by various factors. Unfortunately, CHF has a poor prognosis and a high mortality rate. Recent studies have found that aging is a significant risk factor for the development of CHF and that cellular senescence plays a vital role in its development. This article reviews different types of cellular senescence, mitochondrial dysfunction in senescent cells, autophagy in senescent cells, and senescence-associated secretory phenotype (SASP), and epigenetic regulation, to provide new perspectives on the research and treatment of CHF. • Aging is a key risk factor for chronic heart failure, with cellular senescence driving its progression. • Reviews cellular senescence's role in chronic heart failure pathogenesis and potential therapies. • Covers senescence in cardiac cells (progenitor, cardiomyocyte, endothelial, fibroblast, immune) and key mechanisms. • Targeting senescence-related pathways offers novel therapeutic strategies for chronic heart failure.
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Zhao et al. (2025) studied this question.
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