No abstract

Myocardial infarction is classified as the irreversible myocardial cell death following ischemia. Ischemia could be initiated as a result of atherosclerotic or variable non-atherosclerotic causes. Consequent effects of ischemia are primarily caused due to oxidative stress which is the main precursor of cell death. Myocardial cell death is triggered through intrinsic or extrinsic pathways. In both pathways, apoptosis has been clearly explained through different studies but recently, necroptosis was determined to be involved. The heart has negligible ability for regeneration, thus infarcted regions are healed by replacing dead cells with scar formation. Infarct healing is triggered through an inflammatory cascade, induced by alarmins released from dying cells. Clearance of dead cells by immune cells is followed with the activation of fibroblasts to promote deposition of extracellular matrix proteins. This review discusses the events involved following ischemia including the mechanistic signalling during injury, inflammation, and repair of the infarcted heart. Moreover, the possible complications are mentioned along with the established treatment strategies and some new therapeutic approaches for myocardial infarction.

Understanding the molecular mechanism of bile formation and the different pathways and pathogenesis of drug induced cholestasis provide different possibilities for treatment. This review summarizes the role of transport proteins in hepatic drug clearance and toxicity, the involvement of inflammatory mediators in cholestasis and the role of nuclear receptors in bile acid metabolism. Understanding nuclear receptor function can help in the development of nuclear receptor ligands for treatment of cholestasis.