This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.
Ischemia-reperfusion injury (IRI) occurred when an organ lost its blood supply in a short time, and then the perfusion was restored automatically or iatrogenically, leading to a burst of reactive oxygen species (ROS) from mitochondria. It is common in the clinic, and lead to deterioration, even death, so an exploratory examination of the mechanism of ischemia-reperfusion injury is of great significance. Among the most common and fatal types of IR in myocardial tissue, myocardial IRI is one of the most fatal diseases in the modern world. The cellular and molecular mechanisms of IRI mainly include calcium overload, oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, energy metabolic disorders, neutrophil infiltration, cardiomyocyte autophagy, and apoptosis, etc. The main pathogenesis of IRI is programmed cell death, of which apoptosis is the most deeply studied processes. However, pyroptosis is a highly inflammatory form of programmed cell death (PCD), which depends on the activation of the caspase cascade and inflammatory mediators, which have been thought to be involved in the processes of IRI. Ptosis has been referred to as a pattern. PCD with apoptosis characteristics Necrosis. It’s stimulated by molecular signaling pathways similar to apoptosis, mainly including Caspase. The research progress in recent years is presented in this review. Among them, myocardial tissue and so on provide a theoretical basis for the burning organ system in I/R injury and provide theoretical practice for the clinical research of reducing ischemia-reperfusion injury.
The authors declared that they have no conflicts of interest to this work.