To Explore the Therapeutic Potential of Sigma Receptor Modulators in Experimental Models of Myocardial Injury

Abstract

Ischemic heart disease is regarded as a global burden on healthcare resources, with the potential to become the prime cause of deaths globally in future. Ischemic cardiac illness caused by abrupt coronary occlusion and delayed reperfusion, as well as chemical-induced myocardial injury, culminate in acute myocardial infarction or myocardial ischemic injury. Early restoration of blood is the exclusive way-out for salvage of alive myocardium from anticipated dying. Prompt blood restoration reestablishes the delivery of O2 and produces the substrates of aerobic ATPs. The harmful reactive oxygen species (ROS) triggers during delayed reperfusion of ischemic myocardium. ROS can cause tissue damage by causing mutilation of DNA, lipids oxidative degradation and protein damaging covalent modification. Furthermore, ischemia/ reperfusion injury causes a redox imbalance, making myocytes more venerable to oxidative affliction. Protecting the heart from ischemic damage proved to be a providential strategy for alleviating varied consequences related to coronary disease for overall health equity of human beings as well as society. Several receptors are implicated in ischemia-reperfusion and chemically-evoked myocardial damage. Sigma receptor is one of the major receptor has been ascertained initially in neonatal cardiac myocytes and later in mature rats, and it has been established that stimulation of these receptors directly provoked the inotropic and chronotropic effects of myocytes. Both and#963;-1R and and#963;-2R subtypes were also documented on human cardiac myocytes. newline