Inhibition of EGFR activity is emerging as a potential therapeutic strategy to treat cardiovascular diseases including hypertension, cardiac hypertrophy, renal fibrosis, and abdominal aortic aneurysm.
EGFR transactivation by GPCR agonists is a key pathophysiological mechanism in cardiovascular diseases, making EGFR inhibition a potential therapeutic target.
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.
Forrester et al. (Fri,) conducted a review in Cardiovascular and renal diseases (hypertension, cardiac hypertrophy, renal fibrosis, abdominal aortic aneurysm). EGFR inhibition was evaluated. Inhibition of EGFR activity is emerging as a potential therapeutic strategy to treat cardiovascular diseases including hypertension, cardiac hypertrophy, renal fibrosis, and abdominal aortic aneurysm.
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