Myocardial ischemia/reperfusion injury: Mechanisms of injury and implications for management (Review)

Abstract

Myocardial infarction is one of the primary causes of mortality in patients with coronary heart disease worldwide. Early treatment of acute myocardial infarction restores blood supply of ischemic myocardium and decreases the mortality risk. However, when the interrupted myocardial blood supply is recovered within a certain period of time, it causes more serious damage to the original ischemic myocardium; this is known as myocardial ischemia/reperfusion injury (MIRI). The pathophysiological mechanisms leading to MIRI are associated with oxidative stress, intracellular calcium overload, energy metabolism disorder, apoptosis, endoplasmic reticulum stress, autophagy, pyroptosis, necroptosis and ferroptosis. These interplay with one another and directly or indirectly lead to aggravation of the effect. In the past, apoptosis and autophagy have attracted more attention but necroptosis and ferroptosis also serve key roles. However, the mechanism of MIRI has not been fully elucidated. The present study reviews the mechanisms underlying MIRI. Based on current understanding of the pathophysiological mechanisms of MIRI, the association between cell death-associated signaling pathways were elaborated, providing direction for investigation of novel targets in clinical treatment.

Research progress on effects of traditional Chinese medicine on myocardial ischemia–reperfusion injury: A review

“…The severity of the reperfusion injury is dependent on many factors, such as the length of ischemia time, the temperature and pressure of the perfusion fluid, and the state of ischemic tissues and organs. From the perspective of cardiac function, the resting tension gradually increases with the prolongation of ischemia time, and the developed tension gradually decreases, while the resting tension increases and the developmental tension becomes lower during reperfusion, indicating that the systolic force of the heart decreases diastolic and systolic dysfunction of the heart ( He et al, 2022 ).…”

Counteraction of Myocardial Ferritin Heavy Chain Deficiency by Heme Oxygenase-1

“…These dynamic modulations interact and result in mitochondrial dysfunction, ATP depletion, damage to vital intracellular homeostatic machinery with ensuing myocardial hypercontracture and eventual cardiomyocyte death [ 4 , 8 ]. Several of the aforementioned perturbations are now established components of a distinct form of programmed cell death, namely ferroptosis [ 9 ]. Importantly, a growing body of evidence suggests that ferroptosis is a central pathophysiologic pathway in several cardiovascular diseases, including MI [ 10 , 11 , 12 , 13 ].…”

A novel circulating biomarker lnc‐MALAT1 for acute myocardial infarction: Its relationship with disease risk, features, cytokines, and major adverse cardiovascular events

“…Currently, AMI is often combined with several complications, including arrhythmia and cardiac failure, which induce a huge burden and greatly affect the quality of life among patients 4,5 . Currently, the treatments for AMI mainly include thrombolysis and percutaneous coronary intervention 6,7 . However, the prognosis of a proportion of AMI patients is still dismal 2,8 .…”

“… 4 , 5 Currently, the treatments for AMI mainly include thrombolysis and percutaneous coronary intervention. 6 , 7 However, the prognosis of a proportion of AMI patients is still dismal. 2 , 8 Thus, the exploration of potential convincing biomarkers to reflect disease risk and severity is imperative to promote the management of AMI patients.…”