Our basic science researchers with the Cardiac Surgery Research Program, led by Dr. Subodh Verma, strive to understand the mechanisms of atherosclerosis and to develop novel approaches to treat cardio metabolic diseases.
One of the major area of basic science research in our program focuses on understanding the determinants of endothelial dysfunction, and the interplay between endothelial cell activation, inflammation and atherothrombosis. We have published several key papers which underscore the role of endothelial function in health and disease, and how translational application of measures of vascular health can be used as a biomarker of cardiovascular risk reduction in humans. Recently, work is focusing on evaluating the lncRNAs regulated by hyperglycemia and shear stress in endothelial cells.
We are interested in understanding how impaired DNA damage repair genes affect heart failure and atherosclerosis. Specifically, we are evaluating the role of the DNA damage repair gene BRCA1 in heart failure. Our work has led to 2 US patents on the use of BRCA1 in the treatment of cardiovascular disease, and also highlighted the potential common pathways through which breast cancer and cardiovascular disease may occur.
Our team is actively pursuing how gain and loss of vascular autophagy could be a causal factor in the development of various cardiovascular diseases including atherosclerosis, and aneurysms. We use sophisticated methods of tissue specific genetic knock-out models, and cellular fate tracking to conduct these experiments. Our recent data has revealed a critical role of endothelial autophagy as a regulator of vascular lipid transport.
This is a new area of research that has been developed by Dr. Krishna Singh. Using a variety of elegant techniques, Dr. Singh is evaluating how the primary cilia of endothelial cells may play a role in the development of atherosclerosis and fibrosis through endothelial to mesenchymal transition.
This program has primarily focused on deciphering how various adiopokines (such as adiponectin) can influence the clinical course of vascular dysfunction. This program, co-led by Dr. Hwee Teoh, has made important contributions towards defining the role of adiponectin as a critical regulator of inflammation via modulation of macrophage lineage polarization and microparticle generation and biology as well as sepsis-related mortality.
Led by Dr. Bobby Yanagawa, this program will evaluate the various epigenetic mechanisms of DNA methylation in valvular tissues from patients with rheumatic heart disease.
