期刊
PHARMACOLOGICAL RESEARCH
卷 110, 期 -, 页码 52-64出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2016.05.008
关键词
G protein-coupled receptor; G protein-coupled receptor kinase; Hypertrophy; Heart failure; Myocardium
资金
- National Institute of Health (NIH) [P01HL091799]
- NIH [R37HL061690, R01 HL085503, P01 HL075443, P01 HL108806]
- National Institutes of Health [T32HL091804-CJT]
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. (C) 2016 Elsevier Ltd. All rights reserved.
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