Open AccessLevel of G protein–Coupled Receptor Kinase-2 Determines Myocardial Ischemia/Reperfusion Injury via Pro- and Anti-Apoptotic Mechanisms
Author(s) -
Henriette Brinks,
Matthieu Boucher,
Erhe Gao,
J. Kurt Chuprun,
Stéphanie Pesant,
Philip Raake,
Z. Maggie Huang,
Xiaoliang Wang,
Gang Qiu,
Anna M. Gumpert,
David M. Harris,
Andrea D. Eckhart,
Patrick Most,
Walter J. Koch
Publication year - 2010
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.110.221010
Subject(s) - beta adrenergic receptor kinase , g protein coupled receptor kinase , cardioprotection , protein kinase b , pharmacology , kinase , in vivo , receptor , g protein coupled receptor , reperfusion injury , cardiac function curve , medicine , signal transduction , myocardial infarction , chemistry , endocrinology , biology , heart failure , ischemia , microbiology and biotechnology
Activation of prosurvival kinases and subsequent nitric oxide (NO) production by certain G protein-coupled receptors (GPCRs) protects myocardium in ischemia/reperfusion injury (I/R) models. GPCR signaling pathways are regulated by GPCR kinases (GRKs), and GRK2 has been shown to be a critical molecule in normal and pathological cardiac function.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom