期刊
CIRCULATION RESEARCH
卷 109, 期 2, 页码 217-230出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.110.231225
关键词
beta-arrestin; cardiac contractility; G protein-coupledreceptor; hypertrophy
资金
- National Institutes of Health [R01 HL105414-01]
G protein-coupled receptors signal through a variety of mechanisms that impact cardiac function, including contractility and hypertrophy. G protein-dependent and G protein-independent pathways each have the capacity to initiate numerous intracellular signaling cascades to mediate these effects. G protein-dependent signaling has been studied for decades and great strides continue to be made in defining the intricate pathways and effectors regulated by G proteins and their impact on cardiac function. G protein-independent signaling is a relatively newer concept that is being explored more frequently in the cardiovascular system. Recent studies have begun to reveal how cardiac function may be regulated via G protein-independent signaling, especially with respect to the ever-expanding cohort of beta-arrestin-mediated processes. This review primarily focuses on the impact of both G protein-dependent and beta-arrestin-dependent signaling pathways on cardiac function, highlighting the most recent data that illustrate the comprehensive nature of these mechanisms of G protein-coupled receptor signaling. (Circ Res. 2011;109:217-230.)
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