Dr. Awad laboratory investigates the critical role of macrophages, arginases and Pigment Epithelium Derived Factor (PEDF) that play a pivotal role in the development and progression of diabetic nephropathy. Demonstrating that macrophages, arginases and/or PEDF play a central role in diabetic nephropathy will have important clinical relevance. A number of pharmacological agents could be considered in future trials. ROLE OF ARGINASE-2 IN DIABETIC NEPHROPATHY: Work generated from studying the role of arginase-2 in diabetic nephropathy in Dr. Awad laboratory has been recently published in Diabetes and Kidney International Journals. Our studies demonstrate for the first time that arginase-2 plays an essential role in the development of diabetic nephropathy. This conclusion is based on three novel observations: First, we demonstrated a beneficial effect of arginase inhibition in animal models of diabetic nephropathy. Second, we showed that deficiency specifically of arginase-2 ameliorates diabetic renal injury. Third, we demonstrated that arginase inhibition mediates renal tissue protection in diabetic nephropathy via an eNOS-dependent mechanism. Results of these studies may ultimately result in novel therapeutic interventions designed to attenuate arginase activity or signaling that regulate arginase-2 expression in the treatment of diabetic kidney disease ROLE OF MACROPHAGE IN DIABETIC NEPHROPATHY: Our recent work was published in American Journal of Physiology-Renal Physiology and demonstrates three seminal findings. First, we demonstrated a beneficial effect of a CCR2 antagonist as a novel therapy in the treatment of diabetic nephropathy. Second, we showed for the first time that deficiency of CCR2 (using CCR2 knock out mice) ameliorates monocyte/macrophage-induced diabetic renal injury. Third, using a macrophage reconstitution strategy, we show the first evidence of the direct role of macrophages CCR2 in diabetic nephropathy. We further demonstrated the first evidence for a direct role of macrophages in diabetic nephropathy. We also provided novel evidence for direct podocyte/macrophage interactions and show that M1, but not M2, macrophages impair podocyte integrity.