◀ Back to ANGPT2

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