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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.