According to the World Health Organization (WHO), across the world the total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. The maximum absolute increase in the number of people with diabetes will be in India. In 2000, the number of diabetic patients was the 31 million and is predicted to be increased to 79 million till 2030. Diabetes is characterized by chronic high glucose levels and in the long run development of different pathological alterations in the retina, renal glomerulus, heart, blood vessels and peripheral nerve. Diabetes specific microvascular disease is a leading cause of blindness (retinopathy), renal failure (nephropathy) and nerve damage (neuropathy), and diabetes-accelerated atherosclerosis (vasculopathy) leads to increased risk of myocardial infarction, stroke and finally to heart failure. Out of these abnormalities, diabetic nephropathy is became the world leading cause of chronic and end-stage renal disease. Hence, my area research of interest  is to find out the molecular mechanisms involved in the development of different diabetic complications.

 

Rapid progress within the last few years has brought a wealth of information regarding diverse roles for the covalent modifications of histones during development and differentiation. Histone modifications have been implicated in the regulation of genomic stability, gene expression, heterochromatin formation and developmental pathways. There are a daunting and growing number of histone modifications. The main emphasis has been on identifying modifications and their locations within the genome. However, very little is known about the interplay between the complex machinery that catalyzes the addition or removal of these modifications and how they are involved in orchestrating development. Therefore, we mainly focusing on the development of targeted therapeutics for diabetes and its complications associated with the misregulation of chromatin modifications.