Research Progress on The Mechanism and Treatment of Inflammatory Response in Myocardial Ischemia-Reperfusion Injury


  • Dong Zhang Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University, Yichang 443000, China
  • Hui Wu Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University, Yichang 443000, China
  • Di Liu Institute of Cardiovascular Diseases, China Three Gorges University, Yichang 443000, China
  • Yunzhao Li Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University, Yichang 443000, China
  • Gang Zhou Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University, Yichang 443000, China



Acute myocardial infarction, myocardial ischemia-reperfusion injury, NLR, caspase, interleukin


Acute myocardial infarction can be treated aggressively with intravenous thrombolysis, percutaneous coronary intervention, and coronary artery bypass grafting; however, recanalization can cause myocardial ischemia-reperfusion injury (MIRI). This is an important reason that restricts the treatment effect of patients. After the ischemic myocardium is restored to perfusion, an inflammatory response can occur within minutes and peak within a few days. Many pro-inflammatory cytokines can seriously damage cardiac function. Inflammation can regulate cardiomyocyte apoptosis, autophagy, pyroptosis, and necrosis, and is the main initiating factor leading to MIRI in cardiomyocytes.

This article reviews the mechanism of inflammatory response in the ischemia-reperfusion period after acute myocardial infarction and the clinical value and application prospect of inhibiting inflammatory response in the treatment of acute myocardial infarction.


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How to Cite

ZHANG, D., WU, H., Liu, D., LI, Y. Z., & ZHOU , G. . (2022). Research Progress on The Mechanism and Treatment of Inflammatory Response in Myocardial Ischemia-Reperfusion Injury. The Heart Surgery Forum, 25(3), E462-E468.