The renin–angiotensin hypothesis for the pathogenesis of cardiac allograft vasculopathy

The precise molecular mechanism for the development of cardiac allograft vasculopathy (CAV) after heart transplantation is not known. We, thus, hypothesize that increased activity of renin–angiotensin system (RAS) is important for the progression of CAV. There is evidence to support this concept. RA...

Full description

Saved in:
Bibliographic Details
Published in:International Journal of Cardiology 2004-06, Vol.95 (2), p.123-127
Main Authors: Yousufuddin, Mohammed, Yamani, Mohamad H.
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cardiac allograft vasculopathy
Cardiology. Vascular system
Cardiovascular Diseases - physiopathology
Coronary Disease - physiopathology
Heart Transplantation
Humans
Medical sciences
Pathogenesis
Postoperative Complications - physiopathology
Renin-Angiotensin System
Renin–angiotensin
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The precise molecular mechanism for the development of cardiac allograft vasculopathy (CAV) after heart transplantation is not known. We, thus, hypothesize that increased activity of renin–angiotensin system (RAS) is important for the progression of CAV. There is evidence to support this concept. RAS via its principal effector molecule, angiotensin II exerts multitude of actions on vascular structure and function including regulation of vasomotor tone, cell growth/apoptosis, fibrosis and inflammation, which are particularly relevant to the genesis of atherosclerotic lesions. Risk factors, which increase predisposition to CAD, are known to activate tissue RAS and thus influence its progression. Importantly, CAD risk factors are also associated with accelerated CAV progression after transplantation. Whereas angiotensin converting enzyme (ACE) gene polymorphism increases the predisposition, pharmacological inhibition of RAS seems to reduce the incidence of CAV. These observations may support our hypothesis, provide a plausible explanation for the molecular mechanisms underlying the development of accelerated CAV and has predictions that can be tested.
ISSN:0167-5273
1874-1754
DOI:10.1016/j.ijcard.2003.05.027