PMID- 23962825 OWN - NLM STAT- MEDLINE DCOM- 20140911 LR - 20220318 IS - 1873-2615 (Electronic) IS - 1050-1738 (Print) IS - 1050-1738 (Linking) VI - 24 IP - 2 DP - 2014 Feb TI - Functional role, mechanisms of regulation, and therapeutic potential of regulator of G protein signaling 2 in the heart. PG - 85-93 LID - S1050-1738(13)00113-8 [pii] LID - 10.1016/j.tcm.2013.07.002 [doi] AB - G protein-mediated signal transduction is essential for the regulation of cardiovascular function, including heart rate, growth, contraction, and vascular tone. Regulators of G protein Signaling (RGS proteins) fine-tune G protein-coupled receptor-induced signaling by regulating its magnitude and duration through direct interaction with the alpha subunits of heterotrimeric G proteins. Changes in the RGS protein expression and/or function in the heart often lead to pathophysiological changes and are associated with cardiac disease in animals and humans, including hypertrophy, fibrosis development, heart failure, and arrhythmias. This article focuses on Regulator of G protein Signaling 2 (RGS2), which is widely expressed in many tissues and is highly regulated in its expression and function. Most information to date has been obtained in biochemical, cellular, and animal studies, but data from humans is emerging. We review recent advances on the functional role of cardiovascular RGS2 and the mechanisms that determine its signaling selectivity, expression, and functionality. We highlight key unanswered questions and discuss the potential of RGS2 as a therapeutic target. CI - Copyright (c) 2013 Elsevier Inc. All rights reserved. FAU - Zhang, Peng AU - Zhang P AD - Cardiovascular Research Center, Cardiology Division, Rhode Island Hospital and Alpert Medical School of Brown University, Providence, RI, USA. FAU - Mende, Ulrike AU - Mende U AD - Cardiovascular Research Center, Cardiology Division, Rhode Island Hospital and Alpert Medical School of Brown University, Providence, RI, USA. Electronic address: ulrike_mende@brown.edu. LA - eng GR - R01 HL114784/HL/NHLBI NIH HHS/United States GR - R21 HL113918/HL/NHLBI NIH HHS/United States GR - 5P20RR018728-10/8P20GM103537-10/GM/NIGMS NIH HHS/United States GR - P20 GM103652/GM/NIGMS NIH HHS/United States GR - P20 GM103537/GM/NIGMS NIH HHS/United States GR - R01 HL080127/HL/NHLBI NIH HHS/United States GR - HL113918/HL/NHLBI NIH HHS/United States GR - HL80127/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20130817 PL - United States TA - Trends Cardiovasc Med JT - Trends in cardiovascular medicine JID - 9108337 RN - 0 (RGS Proteins) RN - 0 (RGS2 protein, human) SB - IM MH - Animals MH - Cardiovascular Diseases/genetics/*metabolism/pathology/physiopathology/therapy MH - Humans MH - Molecular Targeted Therapy MH - Myocardium/*metabolism/pathology MH - RGS Proteins/genetics/*metabolism MH - *Signal Transduction PMC - PMC3948174 MID - NIHMS517023 EDAT- 2013/08/22 06:00 MHDA- 2014/09/12 06:00 PMCR- 2015/02/01 CRDT- 2013/08/22 06:00 PHST- 2013/05/16 00:00 [received] PHST- 2013/07/08 00:00 [revised] PHST- 2013/07/10 00:00 [accepted] PHST- 2013/08/22 06:00 [entrez] PHST- 2013/08/22 06:00 [pubmed] PHST- 2014/09/12 06:00 [medline] PHST- 2015/02/01 00:00 [pmc-release] AID - S1050-1738(13)00113-8 [pii] AID - 10.1016/j.tcm.2013.07.002 [doi] PST - ppublish SO - Trends Cardiovasc Med. 2014 Feb;24(2):85-93. doi: 10.1016/j.tcm.2013.07.002. Epub 2013 Aug 17.