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• W2350356301 startingPage "52" @default.
• W2350356301 abstract "Heart failure (HF) is a global epidemic with the highest degree of mortality and morbidity of any disease presently studied. G protein-coupled receptors (GPCRs) are prominent regulators of cardiovascular function. Activated GPCRs are turned off by GPCR kinases (GRKs) in a process known as desensitization. GRKs 2 and 5 are highly expressed in the heart, and known to be upregulated in HF. Over the last 20 years, both GRK2 and GRK5 have been demonstrated to be critical mediators of the molecular alterations that occur in the failing heart. In the present review, we will highlight recent findings that further characterize non-canonical GRK signaling observed in HF. Further, we will also present potential therapeutic strategies (i.e. small molecule inhibition, microRNAs, gene therapy) that may have potential in combating the deleterious effects of GRKs in HF." @default.
• W2350356301 created "2016-06-24" @default.
• W2350356301 creator A5025795420 @default.
• W2350356301 creator A5027300987 @default.
• W2350356301 creator A5075648082 @default.
• W2350356301 creator A5089976835 @default.
• W2350356301 date "2016-08-01" @default.
• W2350356301 modified "2023-09-24" @default.
• W2350356301 title "The expanding GRK interactome: Implications in cardiovascular disease and potential for therapeutic development" @default.
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