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ANGPT2 — SMAD2
Text-mined interactions from Literome
de Boer et al., J Mol Med (Berl) 2004
(Disease Models, Animal...) :
Ang II induced LV remodeling and fibrosis are
dependent on both ERK and
Smad2 activation
Peng et al., Circulation 2005
(Cardiomegaly) :
Ang II increased
Smad2 phosphorylation 3.2+/-0.9-fold ; the ACE inhibitor lowered this to 0.6+/-0.1-fold ( P < 0.001 ), and the mAb blocked this decrease to 2.1+/-0.3 ( P < 0.001, ACE inhibitor versus ACE inhibitor+mAb )
Chen et al., J Am Soc Nephrol 2006
(Hypertrophy...) :
Ang II also
stimulated Smad 2/3 phosphorylation, which was blocked by a selective TGF-beta receptor I kinase inhibitor but not by CRM197
Yang et al., Hypertension 2009
(Disease Models, Animal...) :
Additional studies revealed that, in addition to a late ( 24-hour ) TGF-beta dependent Smad2/3 activation,
Ang II also
induced a rapid activation of
Smad2/3 at 15 minutes and expression of CTGF and collagen I in tubular epithelial cells lacking the TGF-beta gene, which was blocked by the addition of an Ang II type 1 receptor antagonist ( losartan ) and inhibitors to extracellular signal regulated kinase 1/2 ( PD98059 ) and p38 ( SB203580 ) but not by inhibitors to Ang II type 2 receptor ( PD123319 ) or c-Jun N-terminal kinase ( SP600125 ), demonstrating a TGF-beta independent, Ang II type 1 receptor mediated extracellular signal regulated kinase/p38 mitogen activated protein kinase cross-talk pathway in Ang II-mediated CTGF and collagen I expression
Zhang et al., Hypertension 2010
(Fibrosis...) :
Enhanced upregulation of the
Ang II type I receptor and
activation of the transforming growth
factor-beta/Smad and nuclear factor-kappaB signaling pathways may be the mechanisms by which CRP promotes cardiac fibrosis and inflammation under high Ang II conditions