PMID- 21861069
OWN - NLM
STAT- MEDLINE
DCOM- 20120507
LR  - 20231113
IS  - 1573-7241 (Electronic)
IS  - 0920-3206 (Print)
IS  - 0920-3206 (Linking)
VI  - 25
IP  - 5
DP  - 2011 Oct
TI  - LOX-1 and angiotensin receptors, and their interplay.
PG  - 401-17
LID - 10.1007/s10557-011-6331-7 [doi]
LID - 401
AB  - The renin-angiotensin system (RAS) plays an important role in regulating blood 
      pressure, water-salt balance and the pathogenesis of cardiovascular diseases. 
      Angiotensin II (Ang II) is the physiologically active mediator and mediates the 
      main pathophysiological actions in RAS. Ang II exerts the effects by activating 
      its receptors, primarily type 1 (AT1R) and type 2 (AT2R). Most of the known 
      pathophysiological effects of Ang II are mediated by AT1R activation. The precise 
      physiological function of AT2R is still not clear. Generally, AT2R is considered 
      to oppose the effects of AT1R. Lectin-like oxidized low-density lipoprotein 
      scavenger receptor-1 (LOX-1) is one of the major receptors responsible for 
      binding, internalizing and degrading ox-LDL. The activation of LOX-1 has been 
      known to be related to many pathophysiological events, including endothelial 
      dysfunction and injury, fibroblast growth, and vascular smooth muscle cell 
      hypertrophy. Many of these alterations are present in atherosclerosis, 
      hypertension, and myocardial ischemia and remodeling. A growing body of evidence 
      suggests the existence of a cross-talk between LOX-1 and Ang II receptors. Their 
      interplays are embodied in the reciprocal regulation of their expression and 
      activity. Their interplays are involved in a series of signals. Recent studies 
      suggests that reactive oxygen species (ROS), nitric oxide (NO), protein kinase C 
      (PKC) and mitogen activated protein kinases (MAPKs) are important signals 
      responsible for their cross-talk. This paper reviews these aspects of 
      dyslipidemia and RAS activation.
FAU - Wang, Xianwei
AU  - Wang X
AD  - Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, 
      AR 72205, USA. XWang2@UAMS.edu
FAU - Phillips, M Ian
AU  - Phillips MI
FAU - Mehta, Jawahar L
AU  - Mehta JL
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Cardiovasc Drugs Ther
JT  - Cardiovascular drugs and therapy
JID - 8712220
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Scavenger Receptors, Class E)
SB  - IM
MH  - Animals
MH  - Dyslipidemias/metabolism
MH  - Humans
MH  - Receptor, Angiotensin, Type 1/*metabolism
MH  - Receptor, Angiotensin, Type 2/*metabolism
MH  - Renin-Angiotensin System/physiology
MH  - Scavenger Receptors, Class E/*metabolism
PMC - PMC7102029
EDAT- 2011/08/24 06:00
MHDA- 2012/05/09 06:00
PMCR- 2020/03/28
CRDT- 2011/08/24 06:00
PHST- 2011/08/24 06:00 [entrez]
PHST- 2011/08/24 06:00 [pubmed]
PHST- 2012/05/09 06:00 [medline]
PHST- 2020/03/28 00:00 [pmc-release]
AID - 6331 [pii]
AID - 10.1007/s10557-011-6331-7 [doi]
PST - ppublish
SO  - Cardiovasc Drugs Ther. 2011 Oct;25(5):401-17. doi: 10.1007/s10557-011-6331-7.