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Cardiovascular disease is the leading cause of death globally. According to the World Health Organization (WHO), it was responsible for 30% of all deaths in 2005 (Basson, 2008). Cardiovascular disease refers to a generalized term which is characterized by compensated cardiac function. Any cardiovascular disease can lead towards heart failure if it is not taken care of early enough. Heart failure is the condition where the heart is unable to pump sufficient oxygenated blood to the tissues to meet their metabolic needs (Ahumada, 1987).
Cardiac hypertrophy and myocardial infarction (MI) are two very common pathophysiological conditions associated with different forms of cardiac disorders discussed above. According to a study conducted by World Health Organization, these two etiologically different pathophysiological conditions are the major causes of morbidity all over the world at present (World health report, 2008). Although the clinical symptoms associated with these two conditions are well characterized, unfortunately no study has been conducted so far to compare and contrast the molecular changes associated with these two etiologically different conditions.
My graduate work was primarily focused on identification of novel causal proteins and related signaling mechanisms during two etiologically different cardiac disease forms – cardiac hypertrophy and myocardial infarction using murine models. A comparative proteome profile revealed changes in expression of proteins involved in various metabolic pathways, stress responses, contractile machinery, apoptotic signaling and other functions in these two diseases forms. Further downstream pathway analysis revealed that two different organelles mitochondria and endoplasmic reticulum play predominant roles during hypertrophy and MI respectively. Interestingly, I found that a small heat shock protein -- Alpha-Crystallin B (CRYAB) plays the role of a switch molecule that shifts apoptotic load from mitochondria to endoplasmic reticulum in dying cardiomyocytes during MI . At this juncture I tried to dig deep into the regulation of CRYAB and found that P38 MAPK plays the role of a master regulator of CRYAB. It was also revealed during the study that P38 MAPK plays a pro-survival role during myocardial infarction .
Currently I'm working in a project that deals with the regulation of cardiac energy metabolism during hypertrophy and MI.
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