Sandhya Sitasawad Ph.D.
Field of Expertise
National Centre For Cell Science (NCCS), Ganeshkhind, Pune Maharashtra
Dr Sandhya Sitaswad did her M.Sc. in Life Science from School of Life Science, Jawaharlal Nehru University, New Delhi and M.Phil in Radiation Biology from School of Life Science, Jawaharlal Nehru University, New Delhi. She then went on to do a Ph.D in Radiation Biology from School of Life Science, Jawaharlal Nehru University, New Delhi 110067, India. The broad areas of my research include involvement of free radicals in diabetes and cancer. Diabetes induced cardiovascular complications are a major cause of morbidity and mortality in diabetic patients. Of the various cardiovascular complications, Diabetic cardiomyopathy (DCM) characterized by left ventricle (LV) systolic and diastolic dysfunction carries a substantial risk for heart failure and increased mortality in diabetic patients. Several studies have shown hyperglycemia and cell death such as apoptosis playing an important role leading to diabetic cardiomyopathy. However, the molecular mechanisms behind the pathogenesis remain incompletely understood.
Currently, research in my laboratory is focused on elucidating the cellular and molecular mechanisms that underlie the pathogenic processes occurring in the heart leading to diabetic cardiomyopathy. Evidences implicating increased oxidative stress and low antioxidant capacity in the development of diabetic cardiac complications in animals or humans suggest that cellular redox regulation may provide important insights for elucidating the molecular mechanisms underlying altered cardiac function in diabetes.
We are particularly interested in hyperglycemia induced contractile dysfunction and stress signaling changes in diabetic heart. Since the cytotoxic actions of glucose are mediated, in part, through oxidative stress and intracellular Ca2+ overload, the focus of our work is to study the role of oxidative and nitrosative stress and calcium regulation in diabetic cardiomyopathy. We are currently focused on understanding the role of mitochondrial Monoamine Oxidase-A (MAO-A) and the antioxidant Peroxiredoxin-3 through Thioredoxin-2 as well as Nrf2 mediated antioxidant mechanisms in hyperglycemia-induced oxidative stress in diabetic cardiomyopathy.