The role of cFLIP in cardiac remodeling post myocardial infarction

Background and Rationale: The role of a master apoptosis regulator, FLIP (FLICE-inhibitory protein), member of the TNF signaling pathway, in the process of remodeling following myocardial infarction (MI) leading to heart failure is unknown. Binding of TNFα to its receptor results in the rapid recruitment of FADD (Fas-associated death domain protein) and procaspase-8 forming the “death-inducing signaling complex” (DISC) triggering a caspase cascade leading to cell death. FLIP is an antiapoptotic protein, recruited to the DISC, interferes with the recruitment of procaspase-8, thereby inhibiting apoptosis.