Research Progress on the Role and Mechanism in the Change of Cardiac Structure and Function of Cardiac Fibrosis in the Elderly.
Abstract
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.
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
The paper discusses the mechanisms of cardiac fibrosis and its role in diastolic heart failure in the elderly. This research is relevant as it addresses age-related changes in cardiac function, which are critical to understanding and potentially mitigating the effects of aging on heart health.
Author of this paper? Send a correction.