<p>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.</p>