期刊
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, VOL 56
卷 56, 期 -, 页码 627-653出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-pharmtox-070115-095427
关键词
angiotensin II; aldosterone; vascular smooth muscle; endothelium; heart; kidney; signal transduction
资金
- NHLBI NIH HHS [R01 HL133248, HL128324] Funding Source: Medline
- NIDDK NIH HHS [R01 DK051265, R01 DK095785] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL128324, R01HL133248] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK051265] Funding Source: NIH RePORTER
Epidermal growth factor receptor (EGFR) activation impacts the physiology and pathophysiology of the cardiovascular system, and inhibition of EGFR activity is emerging as a potential therapeutic strategy to treat diseases including hypertension, cardiac hypertrophy, renal fibrosis, and abdominal aortic aneurysm. The capacity of G protein-coupled receptor (GPCR) agonists, such as angiotensin II (AngII), to promote EGFR signaling is called transactivation and is well described, yet delineating the molecular processes and functional relevance of this crosstalk has been challenging. Moreover, these critical findings are dispersed among many different fields. The aim of our review is to highlight recent advancements in defining the signaling cascades and downstream consequences of EGFR transactivation in the cardiovascular renal system. We also focus on studies that link EGFR transactivation to animal models of the disease, and we discuss potential therapeutic applications.
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