1. HO-1/EET and Metabolic Syndrome / Diabetes. HO acts as a molecular “switch” to genetically reprogram adipocyte stem cells and subsequently, vascular endothelium through activation of a unique signaling cascade that results in the amplification of protective circuits, including EET, and provides resistance to vascular dysfunction. 1. Gene targeting, hypertension and vascular function. Based on the beneficial anti-oxidative and anti-inflammatory function of HO-1, we assess the contribution of tissue-specific HO-1 cytoprotective properties to the pathogenesis of disease in which oxidative stress has been implicated. 1. HO-1/EET Gene Targeting to EC / Adipocytes. Targeting adipose tissue using the adipocyte-specific vector, (LV-aP2-HO-1) elicited long-term endothelium protection with sustained elevated levels of the EET-adiponectin-pAMPK-signaling pathway and amelioration of obesity-mediated hypertension. 4. PGC1α as the Mediator of the HO-EET Anti-adipogenic Properties Recently, studies in my lab uncovered evidence that the interplay of HO-1 and EETs modulates the adipocyte phenotype by regulating peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), a transcription factor and a master regulator of mitochondrial biogenesis and insulin sensitivity; it plays a critical role in the regulation of adipogenesis and in transforming white fat to brown fat-like adipocytes.