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10.1146/annurev-pharmtox-070115-095427

http://scihub22266oqcxt.onion/10.1146/annurev-pharmtox-070115-095427
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C5477061!5477061!26566153
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suck abstract from ncbi


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pmid26566153      Annu+Rev+Pharmacol+Toxicol 2016 ; 56 (ä): 627-53
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  • EGFR transactivation: mechanisms, pathophysiology and potential therapies in cardiovascular system #MMPMID26566153
  • Forrester SJ; Kawai T; Elliott KJ; O?Brien S; Thomas W; Harris RC; Eguchi S
  • Annu Rev Pharmacol Toxicol 2016[]; 56 (ä): 627-53 PMID26566153show ga
  • Accumulating studies suggest that the epidermal growth factor receptor (EGFR) activation is associated with 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 well described ? a process termed EGFR ?transactivation? ? 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 the recent advancement of the signaling cascades and downstream consequences of EGFR transactivation within the cardiovascular renal system in vitro and in vivo. We will also focus on linking EGFR transactivation to animal models of the disease as well as the potential therapeutic applications.
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