Abstract
Ischemia-reperfusion (I/R) injury is a manifestation of tissue or organ damage that is followed by ischemia and exacerbated by the return of blood flow to a previously damaged tissue or organ. The intestines are one of the most sensitive tissues and organs to I/R injury. Moreover, the adverse consequences of intestinal I/R (II/R) injury are not limited to the intestine itself and can also lead to damage of the distant tissues and organs. The mechanism of II/R is extremely complex and oxidative stress is the key link in the pathogenesis of II/R injury. This study summarizes the roles of oxidative stress and its signaling pathways involved in II/R. The signaling pathways that mitigate II/R injury include the nuclear factor erythroid-related factor 2 (Nrf2)-mediated signaling pathway, Wnt/β-catenin pathway, and phosphatidylinositol kinase 3 (PI3K)/Akt pathway; those that aggravate II/R injury include the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, Toll-like receptor (TLR) receptor-mediated signaling pathway, protein kinase CβII (PKCβII)/p66shc pathway, and microRNA (miRNA)/p66shc pathway; the effect of miRNA on related pathways and mitochondrial DNA translocation. The aforementioned pathways provide new ideas for further exploring the occurrence and development of II/R and more effective treatments for II/R injury.
Highlights
Ischemia-reperfusion (I/R) injury is a serious clinical event
This study focuses on the oxidative stress and II/R and a search of the Medical Subject Headings (MeSHs) was carried out using PubMed as follows: oxidative stress, intestinal, gut, and I/R
As oxygen is restored during reperfusion, abundant reactive oxygen species (ROS) in damaged cells and tissues can attack almost all the intracellular biomolecules and this oxidative stress disrupts the dynamic homeostasis of the epithelial cells through signal transduction pathways, thereby resulting in the release of large amounts of inflammatory mediators and the induction of apoptosis and exacerbating the damage after reperfusion [6]
Summary
Ischemia-reperfusion (I/R) injury is a manifestation of tissue or organ damage that is followed by ischemia and exacerbated by the return of blood flow to a previously damaged tissue or organ. The intestines are one of the most sensitive tissues and organs to I/R injury. The adverse consequences of intestinal I/R (II/R) injury are not limited to the intestine itself and can lead to damage of the distant tissues and organs. The mechanism of II/R is extremely complex and oxidative stress is the key link in the pathogenesis of II/R injury. This study summarizes the roles of oxidative stress and its signaling pathways involved in II/R. The aforementioned pathways provide new ideas for further exploring the occurrence and development of II/R and more effective treatments for II/R injury
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