Cardiovascular disease (CVD) is the leading cause of death in the world, accounting for 30% of all deaths (17). The identification of novel biomarkers indicating the progression, or signaling pathways which can be exploited as a treatment for CVD is a subject of ongoing interest for combating this disease. It is well established that obesity is a leading risk factor for CVD (63), however very little attention has been given to the endocrine function of adipose tissue and its role in CVD. In both cell culture and animal models CTRP3 has been shown to be protective following heart attack (myocardial infarction, MI) or stroke (intracerebral hemorrhage, ICH) (11,42,67,77,80,81,83,89). Table 6 contains the complete summary of the treatment effects of CTRP3 treatment as it related to CVD. Specifically, CTRP3 stimulates mitochondrial biogenesis in cardiac tissue and promotes vascular relaxation (85,89), whereas 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
