Our research focus is to understand the molecular mechanisms regulating vascular endothelial function and its significance in the development of atherosclerosis. Our current work is aimed at identifying how sumoylation controls vascular function and whether endothelial sumoylation contributes to the development of atherosclerosis. Increasing sumoylation in vasculature is known to impair endothelial capacity to relax blood vessels and accelerate the development of atherosclerosis. We aim to identify the mechanism via which sumoylation, more specifically SUMO2, regulates endothelial function and determine the pathways involved. We use multiple approaches including cellular and molecular biology assays and genetic mouse models to study the impact of our target protein on the vascular function. Our work is expanding, people with interested in vascular biology research are welcome to join our team.
Kumar S. Physical activity pacifies the problematic p66Shc. Eur J Prev Cardiol. 2020 Jan;27(2):166-167. PMID: 31707837.
Kim YR, Jacobs JS, Li Q, Gaddam RR, Vikram A, Liu J, Kassan M, Irani K, Kumar S. SUMO2 regulates vascular endothelial function and oxidative stress in mice. Am J Physiol Heart Circ Physiol. 2019 Dec 1;317(6):H1292-H1300. PMID: 31584834. Selected for APSselect.
Kumar S. P66Shc and vascular endothelial function. Biosci Rep. 2019 Apr 30;39(4):BSR20182134. PMID: 30918103.
Kumar S, Kim YR, Vikram A, Naqvi A, Li Q, Kassan M, Kumar V, Bachschmid MM, Jacobs JS, Kumar A, Irani K. Sirtuin1-regulated lysine acetylation of p66Shc governs diabetes-induced vascular oxidative stress and endothelial dysfunction. Proc Natl Acad Sci U S A. 2017 Feb 14;114(7):1714-1719. PMID: 28137876