Androgen modulates cardiac fibrosis contributing to gender differences on heart failure.
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.
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Cheng-Chih
CC
Chung
Yu-Hsun
YH
Kao
Yu-Ju
YJ
Chen
Yi-Jen
YJ
Chen
D000728:Androgens / Q000172:deficiency / Q000502:physiology*; D000804:Angiotensin II / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009206:Myocardium / Q000473:pathology*; D018384:Oxidative Stress / Q000502:physiology; D012737:Sex Factors; D013624:Taiwan; D016212:Transforming Growth Factor beta / Q000378:metabolism / Q000502:physiology; D055815:Young Adult
D000728:Androgens; D016212:Transforming Growth Factor beta; D000804:Angiotensin II