My research activities are focused on the fundamental mechanisms of the development of atherosclerosis and heart failure. Specifically, I am interested in studying the role of oxidative stress in the development of cardiovascular diseases and associated risk factors including Type 2 diabetes. In addition, I am interested in both the prevention and cure of cardiovascular diseases using nutritional, pharmacological, and life style modulations.
Several years ago I proposed the oxidative theory of atherosclerosis, which has gained considerable acceptance, and as a result a substantial population consumes antioxidant vitamins. However, a number of anti-atherogenic behavior traits are themselves pro-oxidant in nature. For example, exercise, a well-known deterrent of cardiovascular disease, is known to induce oxidative changes and deplete tissue antioxidants. Similarly, the consumption of polyunsaturated fatty acids, which are more oxidation labile, decreases the progression of atherosclerosis. Based on our recent studies we postulated that a threshold oxidative stress might activate arterial wall antioxidant enzymes, and thus could become anti-atherogenic.
Human arteriosclerotic disease is different from that of animals. We are currently studying the mechanisms involved in the generation of advanced lesions and how calcification and inflammation might affect plaque vulnerability. Some of the ongoing studies in the laboratory include, studies on novel mechanistic insights on the cardio-protective role of aspirin, the use of sesame oil to control plaque progression, role of macrophage adherence in plaque development, progression of oxidative stress and aortic calcification, mechanisms involved in heart failure, and the pathobiology of type 2 diabetes.