This review highlights the role of androgen in modulating cardiac fibrosis via TGF-β, offering mechanistic insights into gender differences in heart failure.
Supports hypothesis of androgen-TGF-β axis in sex-specific heart failure fibrosis; leaves open clinical translation pending prospective trials.
Chronic heart failure (HF) is a major health problem throughout the world. Gender has significant effects on the pathophysiology of HF. Low levels of free testosterone are independently associated with increased chronic HF symptoms and mortality. Cardiac fibrosis plays a pivotal role in structural remodeling in HF. Transforming growth factor (TGF)-β, angiotensin II and oxidative stress contribute to the activity/extent of cardiac fibrosis. Androgen deficiency can up-regulate TGF-β expression under angiotensin II stimulation in vivo. In this review, we summarized the potential mechanisms accounting for the effects of androgen on cardiac fibrosis through regulating fibrocytes activity under TGF, which can explain wound healing and cardiac fibrosis in male with acute myocardial injury and chronic HF.
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Chung et al. (2013) studied this question.
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