Abstract
Local hematopoietic bone marrow (BM) renin-angiotensin system (RAS) affects the growth, production, proliferation differentiation, and function of hematopoietic cells. Angiotensin II (Ang II), the dominant effector peptide of the RAS, regulates cellular growth in a wide variety of tissues in pathobiological states. RAS, especially Ang II and Ang II type 1 receptor (AT1R), has considerable proinflammatory and proatherogenic effects on the vessel wall, causing progression of atherosclerosis. Recent investigations, by analyzing several BM chimeric mice whose BM cells were positive or negative for AT1R, disclosed that AT1R in BM cells participates in the pathogenesis of atherosclerosis. Therefore, AT1R blocking not only in vascular cells but also in the BM could be an important therapeutic approach to prevent atherosclerosis. The aim of this paper is to review the function of local BM RAS in the pathogenesis of atherosclerosis.
Highlights
The renin-angiotensin system (RAS) plays a crucial role in the control of blood pressure, blood flow, fluid volume, and electrolyte balance, and overactivity of this system contributes to the pathogenesis of a variety of clinical conditions, including onset, progression, and outcome of atherosclerosis [1,2,3]
Angiotensinogen (AGT) produced in the liver is the precursor of angiotensin I (Ang I), an inactive decapeptide that is converted into Angiotensin II (Ang II), the main effector of the RAS
Ang II plays a main role in the RAS mediated mainly by two seven transmembrane domain receptors termed Ang II type 1 receptor (AT1R) and Ang II type 2 receptor (AT2R) showing a complex pattern of regulation and function [5]
Summary
The renin-angiotensin system (RAS) plays a crucial role in the control of blood pressure, blood flow, fluid volume, and electrolyte balance, and overactivity of this system contributes to the pathogenesis of a variety of clinical conditions, including onset, progression, and outcome of atherosclerosis [1,2,3]. Most of the well-known actions of Ang II-AT1R interaction causes vasoconstriction and aldosterone release from the adrenal gland This classical description of the RAS has been expanded by recent findings that RAS is activated locally, in the vessel wall, heart, the kidney, and the brain [6,7,8,9,10,11,12,13,14]. Fukuda and Sata [21] proposed a hypothesis that the local RAS in BM plays crucial roles in atherosclerosis They have demonstrated that Ang II-AT1R pathway in BM contributes to atherosclerotic development in the hypercholesterolemic mice. The aim of this paper is to outline the function of local BM RAS during the course of progression and destabilization of atherosclerosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
