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ANGPT2 — CASP3

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Foo et al., J Cell Physiol 2006 (Hypertrophy) : Our findings demonstrate that Ang II ( 100 nM, 24 h ) alone upregulates HO-1 expression and induces both myocyte hypertrophy and apoptosis, assessed by measuring terminal deoxynucleotidyltransferase dUTP nick-end labelling ( TUNEL ) staining, caspase-3 activity and mitochondrial membrane potential
Eley et al., Am J Physiol Endocrinol Metab 2008 (Muscular Atrophy) : These results suggest that TNF-alpha/IFN-gamma and ANG II induce muscle protein degradation by a common signaling pathway, which is attenuated by HMB, and that this involves the initial activation of caspase-3 and -8 , followed by autophosphorylation and activation of PKR, which then leads to increased ROS formation via activation of p38 MAPK
Tan et al., Circ Res 2009 (Carotid Artery Injuries...) : Ang II increased SMC apoptosis in an Ang II type 2 receptor-, caspase 8-, and FasL dependent fashion
Parborell et al., Mol Cell Endocrinol 2011 : Moreover, ANGPT1 inhibition increased the levels of active caspase 3 and androsterone, but decreased estradiol, AKT phosphorylation and the area of smooth muscle cell actin
Ren et al., Journal of biomedical research 2012 : Specifically, angiopoietin-1 prevented DOX induced increases in FasL and Bax levels and cleaved caspase-3 and caspase-8 levels in H9C2 cells