【摘 要】
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It is now well accepted that TGF-β/Smad signaling is a major pathway leading to cardiac fibrosis.We recently found under hypertensive conditions, angiotensin Ⅱ is able to activate the TGF-β/Smad signa
【机 构】
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Department of Medicine and Therapeutics, and Li Ka Shing Institute of Health Sciences, The Chinese U
【出 处】
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第17届中国南方国际心血管病学术会议
论文部分内容阅读
It is now well accepted that TGF-β/Smad signaling is a major pathway leading to cardiac fibrosis.We recently found under hypertensive conditions, angiotensin Ⅱ is able to activate the TGF-β/Smad signaling pathway via both TGF-β-dependent and independent mechanisms.Under disease conditions, cardiacSmad3 is highly activated, which is associated with a loss of Smad7, an inhibitor of Smad2/3.The pathogenic role of Smad3 in cardiac fibrosis is examined in hypertensive cardiac disease induced in Smad3 by subcutaneous angiotensin Ⅱ infusion.Results show that deletion of Smad3 prevents angiotensin Ⅱ-mediated cardiac inflammation and fibrosis.
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