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10.1146/annurev-pharmtox-070115-095427

http://scihub22266oqcxt.onion/10.1146/annurev-pharmtox-070115-095427
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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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  • Epidermal Growth Factor Receptor Transactivation: Mechanisms, Pathophysiology, and Potential Therapies in the Cardiovascular System #MMPMID26566153
  • Forrester SJ ; Kawai T ; O'Brien S ; Thomas W ; Harris RC ; Eguchi S
  • Annu Rev Pharmacol Toxicol 2016[]; 56 (ä): 627-53 PMID26566153 show ga
  • 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.
  • |Animals [MESH]
  • |Cardiovascular System/*metabolism [MESH]
  • |ErbB Receptors/*metabolism [MESH]
  • |Humans [MESH]
  • |Signal Transduction/*physiology [MESH]


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