Mitochondrial function in intestinal ischemia-reperfusion injury: mechanisms and therapeutic perspectives.

Intestinal ischemia-reperfusion injury is a common pathophysiological event in acute abdominal conditions, characterized by tissue damage, a systemic inflammatory response, and multiple organ dysfunction. Recent studies have highlighted the central role of mitochondrial dysfunction in the initiation and progression of intestinal ischemia-reperfusion injury. Mitochondria play a crucial role in energy metabolism, redox balance, and cell death signaling, making them significant targets for research and therapeutic interventions. Moreover, oxidative stress-induced mitochondrial dysfunction-manifested by excessive reactive oxygen species production, loss of membrane potential, and calcium imbalance-further exacerbates cellular damage and promotes inflammatory responses. This review systematically examines the pathological mechanisms through which mitochondria contribute to intestinal ischemia-reperfusion injury and explores potential therapeutic strategies targeting mitochondrial function. Future research should focus on integrating signaling pathway analysis with multi-level treatment strategies, fostering the translation of basic research into clinical practice, and ultimately providing both theoretical and practical frameworks for improving patient outcomes.