Oxidative Stress in Intestinal Ischemia-Reperfusion

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/beta-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 C beta II (PKC beta II)/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.

Automated summary

Intestinal ischemia-reperfusion (II/R) injury not only affects the intestine itself, but can also lead to damage of distant tissues and organs. Oxidative stress plays a crucial role in the pathogenesis of II/R injury, and various signaling pathways have different effects on II/R injury.