The Research And Treatment Progress Of Endoplasmic Reticulum Stress After Myocardial Infarction

Ischemic necrosis of myocardial tissue and cells leads to myocardialinfarction (MI). With the improvement of living standards, there is anincreasing trend in the incidence of MI. MI induced heart failure andarrhythmia are the most common complications result in cardiac death.Recent studies demonstrated the pathophysiological changes andventricular remodeling in heart failure after MI. Due to ventricularmyocardial injury, ventricular remodeling can cause a series of changes inthe size, structure and shape of ventricle, the basic pathophysiology changeis related to myocardial apoptosis, inflammation, and myocardial fibrosisespecially to apoptosis. After MI, numerous oxygen free radical generationand unbalanced calcium homeostasis in myocardial cells lead tointracellular protein synthesis disorders through a series of transmembranesignal transduction, induce endoplasmic reticulum stress, persistentendoplasmic reticulum stress can cause misfolded proteins exceeds itsnormal self-cleaning capacity, result in apoptosis of myocardial cells,eventually develop into heart failure. So endoplasmic reticulum stress may be potential treatment target, through regulate endoplasmic reticulum stress,may decrease myocardial apoptosis and inhibit ventricular remodeling,prevent complications after MI. Therefore,to understand the mechanism ofendoplasmic reticulum stress and development new drugs may be veryimportant to improve the prognosis of post-myocardial infarction.