The renin-angiotensin hypothesis for the pathogenesis of cardiac allograft vasculopathy.
作者： Mohammed Yousufuddin , Mohamad H. Yamani
DOI: 10.1016/J.IJCARD.2003.05.027
关键词:
摘要: The precise molecular mechanism for the development of cardiac allograft vasculopathy (CAV) after heart transplantation is not known. We, thus, hypothesize that increased activity renin-angiotensin system (RAS) important progression CAV. There evidence to support this concept. RAS via its principal effector molecule, angiotensin II exerts multitude actions on vascular structure and function including regulation vasomotor tone, cell growth/apoptosis, fibrosis inflammation, which are particularly relevant genesis atherosclerotic lesions. Risk factors, increase predisposition CAD, known activate tissue thus influence progression. Importantly, CAD risk factors also associated with accelerated CAV transplantation. Whereas converting enzyme (ACE) gene polymorphism increases predisposition, pharmacological inhibition seems reduce incidence These observations may our hypothesis, provide a plausible explanation mechanisms underlying has predictions can be tested.
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