Itaconate modulates tricarboxylic acid and redox metabolism to mitigate reperfusion injury

ConclusionsWe hypothesize that itaconate transiently inhibits SDH to gradually “awaken” mitochondrial function upon reperfusion that minimizes ROS and tissue damage. Collectively, our data indicate that itaconate acts as a mitochondrial regulator that controls redox metabolism to improve physiological outcomes associated with IR injury.
Source: Molecular Metabolism - Category: Endocrinology Source Type: research