Heat Stress-Induced Intestinal Barrier Impairment: Current Insights into the Aspects of Oxidative Stress and Endoplasmic Reticulum Stress.
This review presents recent advances in mechanisms of oxidative stress-associated ERS in response to HS, which is destructive to intestinal barrier integrity and the involvement of autophagy and ferroptosis in ERS.
Abstract
Heat stress (HS) occurs when the sensible temperature of animals exceeds their thermoregulatory capacity, a condition that exerts a detrimental impact on health and growth. The intestinal tract, as a highly sensitive organ, has been shown to respond to HS by exhibiting mucosal injury, intestinal leakage, and disturbances in the gut microbiota. Oxidative stress and endoplasmic reticulum stress (ERS) are both potential outcomes of long-term exposure to high temperatures and have been linked to apoptosis, autophagy, and ferroptosis. In addition, HS alters the composition of the gut microbiota accompanied by changed levels of bacterial components and metabolites, rendering the gut more vulnerable to stress-related injury. In this review, we present recent advances in mechanisms of oxidative stress-associated ERS in response to HS, which is destructive to intestinal barrier integrity. The involvement of autophagy and ferroptosis in ERS was highlighted. Further, we summarize the relevant findings regarding the engagement of gut microbiota-derived components and metabolites in modulation of intestinal mucosal injury induced by HS.