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THE ROLE OF MATRIX METALLOPROTEINASES INDUCED ANGIOGENESIS DURING TRANSITION FROM COMPENSATORY CARDIAC HYPERTROPHY TO CARDIAC FAILURE: THERAPEUTIC EFFECTS OF HYDROGEN SULFIDE. Dr.Srikanth Givvimani M.D July 26 2010 Background: Although matrix metalloproteinase (MMPs) and tissue inhibitor of metalloproteinase (TIMPs) playa vital role in tumor angiogenesis and TIMP-3 causes apoptosis, their role in cardiac angiogenesis is unknown. Interestingly, a disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure, however, the proteolytic and anti-angiogenic mechanisms of transition from compensatory hypertrophy to decompensatory heart failure are unclear. Previous studies have shown the cardio protective role of hydrogen sulfide (H2S) in myocardial ischemia, infarction and heart failure, but its role during transition from compensatory cardiac hypertrophy to heart failure is yet to be unveiled. We hypothesize that in pathological pressure overload of the heart, cardiac matrix remodeling is induced by an increase in angiogenic growth factors during the compensatory hypertrophy phase and an increase in antiangiogenic factors during the decompensatory heart failure phase. H2S mitigates

The role of matrix metalloproteinases induced angiogenesis during transition from compensatory cardiac hypertrophy to cardiac failure : therapeutic effects of hydrogen sulfide.