Key result
Age-related cardiac fibrosis contributes to elderly diastolic heart failure via RAAS, ROS, and TGF-β.
Why the study?
Heart failure is closely related to aging, and age-related cardiac fibrosis plays an important role in the pathogenesis of diastolic heart failure.
This review highlights the mechanistic role of age-related cardiac fibrosis, mediated by pathways such as RAAS and TGF-β, in the development of diastolic heart failure in elderly patients.
Suggests antifibrotic targets merit trials in elderly HFpEF; leaves open outcome impact.
Heart failure is closely related to aging. Elderly patients with heart failure are often able to retain normal systolic function, manifested by left ventricular hypertrophy with decreased diastolic function. Relevant studies have shown that age-related cardiac fibrosis plays an important role in the pathogenesis of cardiac diastolic heart failure. Activation of fibroblasts in the heart, the acquisition of a pro-fibrotic phenotype, and age-dependent accumulation of collagen can lead to progressive increases in myocardial stiffness and impaired diastolic function. The renin-angiotensin-aldosterone system, reactive oxygen species, and angiotensin II are closely related to fibrotic remodeling of the heart in the elderly, and their pro-fibrotic effects may be mainly mediated by transforming growth factor β. In this review, we summarize the research progress of the role and mechanism of cardiac fibrosis in the structural and functional changes of the elderly.
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Xiao et al. (2025) conducted a review in Cardiac fibrosis and heart failure in the elderly. Age-related cardiac fibrosis, mediated by RAAS, ROS, and Ang II via TGF-β, plays an important role in the pathogenesis of diastolic heart failure in the elderly.
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