Endothelial Damage and Regeneration: The Role of the Renin-Angiotensin-Aldosterone System

被引:44
作者
Becher, Ulrich M. [1 ]
Endtmann, Cathleen [1 ]
Tiyerili, Vedat [1 ]
Nickenig, Georg [1 ]
Werner, Nikos [1 ]
机构
[1] Univ Klinikum Bonn, Med Klin & Poliklin 2, Sigmund Freud Str 25, D-53105 Bonn, Germany
关键词
Endothelial regeneration; Endothelial damage; Endothelial progenitor cells; EPC; Renin-angiotensin-aldosterone system (RAAS); Endothelial dysfunction; Atherosclerosis; Angiotensin II; Ang II; Angiotensin II receptor blocker; ARB; Angiotensin-converting enzyme inhibitor; ACE inhibitor; Direct renin inhibitor; DRI; PROGENITOR-CELL FUNCTION; INDUCED ATHEROSCLEROSIS; INHIBITION; DISEASE; RISK; NEOANGIOGENESIS; INFLAMMATION; TELMISARTAN; SENESCENCE; EXPRESSION;
D O I
10.1007/s11906-010-0171-x
中图分类号
R6 [外科学];
学科分类号
100210 [外科学];
摘要
The renin-angiotensin-aldosterone system (RAAS) is part of the blood pressure regulating system. Its main effector peptide is angiotensin II (Ang II). Although it may induce hypertension, the proinflammatory, profibrotic, and prothrombotic effects are mainly mediated by effects of Ang II on the cellular and molecular level that are independent of blood pressure. Therefore, pharmacotherapeutic intervention within the RAAS is an important treatment modality for patients suffering from cardiovascular diseases, even those who are not hypertensive. In addition to the blood pressure lowering and vasculoprotective (pleiotropic) effects of angiotensin II type 1 (AT(1)) receptor blockers (ARBs), and angiotensin-converting enzyme (ACE) inhibitors, regenerative progenitor cell therapy emerges as an auxiliary therapy to improve regeneration of the vascular endothelium. This review focuses on the growing knowledge about regenerating vascular cells, their response to RAAS effectors, and RAAS-modulating pharmacotherapy in the context of endothelial cell damage and regeneration.
引用
收藏
页码:86 / 92
页数:7
相关论文
共 52 条
[1]
Abali Huseyin, 2002, Hematology, V7, P75, DOI 10.1080/10245330290022160
[2]
[Anonymous], 2000, Lancet, V355, P253, DOI [10.1016/S0140-6736(99)12323-7, DOI 10.1016/S0140-6736(99)12323-7]
[3]
Isolation of putative progenitor endothelial cells for angiogenesis [J].
Asahara, T ;
Murohara, T ;
Sullivan, A ;
Silver, M ;
vanderZee, R ;
Li, T ;
Witzenbichler, B ;
Schatteman, G ;
Isner, JM .
SCIENCE, 1997, 275 (5302) :964-967
[4]
Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization [J].
Asahara, T ;
Masuda, H ;
Takahashi, T ;
Kalka, C ;
Pastore, C ;
Silver, M ;
Kearne, M ;
Magner, M ;
Isner, JM .
CIRCULATION RESEARCH, 1999, 85 (03) :221-228
[5]
Stimulation of endothelial progenitor cells - A new putative therapeutic effect of angiotensin II receptor antagonists [J].
Bahlmann, FH ;
de Groot, K ;
Mueller, O ;
Hertel, B ;
Haller, H ;
Fliser, D .
HYPERTENSION, 2005, 45 (04) :526-529
[6]
Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors [J].
Case, Jamie ;
Mead, Laura E. ;
Bessler, Waylan K. ;
Prater, Daniel ;
White, Hilary A. ;
Saadatzadeh, M. Reza ;
Bhavsar, Janak R. ;
Yoder, Mervin C. ;
Haneline, Laura S. ;
Ingram, David A. .
EXPERIMENTAL HEMATOLOGY, 2007, 35 (07) :1109-1118
[7]
Bone marrow transplantation reveals that recipient AT1a receptors are required to initiate angiotensin II-induced atherosclerosis and aneurysms [J].
Cassis, Lisa A. ;
Rateri, Debra L. ;
Lu, Hong ;
Daugherty, Alan .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2007, 27 (02) :380-386
[8]
Cheng S, 2010, CIRCULATION 0907
[9]
Effect of Direct Renin Inhibition on Renal Hemodynamic Function, Arterial Stiffness, and Endothelial Function in Humans With Uncomplicated Type 1 Diabetes - A pilot study [J].
Cherney, David Z. I. ;
Lai, Vesta ;
Scholey, James W. ;
Miller, Judith A. ;
Zinman, Bernard ;
Reich, Heather N. .
DIABETES CARE, 2010, 33 (02) :361-365
[10]
Endothelial colony-forming cell role in neoangiogenesis and tissue repair [J].
Critser, Paul J. ;
Yoder, Mervin C. .
CURRENT OPINION IN ORGAN TRANSPLANTATION, 2010, 15 (01) :68-72