immediately following a MI there is a significant decrease of adipose tissue CTRP3 mRNA and circulating CTRP3 protein levels (77, 81). In animals models of MI exogenous CTRP3 pretreatment (adenovirus-delivered or recombinant CTRP3) increases survival, improves postevent cardiac function, and prevents pathological remodeling (77, 81). Progressive remodeling after myocardial infarction (MI) is a leading cause of morbidity and mortality associated with MI. Specifically Transforming growth factor beta (TGF-β) has been reported to be involved in ventricular remodeling by promoting myocardial fibrosis (88). However, CTRP3 attenuates TGF-β1-induced signaling and pathogenic remodeling post-MI both in vivo and in vitro (77). Regarding stroke recovery, preconditioning with CTRP3 reduced cerebral edema, reduced blood-brain barrier damage, improved neurological function, and reduced oxidative stress following ICH (67,80). Collectively, these data illustrate the potential of CTRP3 and CTRP3-mediated signaling pathways as a prospective post-MI/ICH treatment targets.
