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Updated: Sep 9, 2025
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Orchestrating cellular fate: Post-Translational modifications as master regulators and therapeutic targets in
Xu Zhong1, Fei-Xiang Wang1, Dan-Ni Chen2
1Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, 646000, China; Anesthesiology and Critical Care Medicine Key Laboratory of Luzhou, Southwest Medical University, Luzhou, Sichuan, 646000, China.
Intestinal ischemia-reperfusion injury (IIRI) represents a severe acute abdominal condition characterized by high mortality and multifaceted pathophysiological mechanisms. The principal features include tissue oxygen deficiency during ischemic phases followed by intensified oxidative stress during reperfusion, resulting in intestinal mucosal barrier dysfunction, inflammatory mediator release, and cellular death pathways activation. Recent advances have highlighted the significance of post-translational modifications (PTMs) in regulating protein functionality. This review explores various key PTMs (phosphorylation, acetylation, methylation, ubiquitination, and glycosylation) and their involvement in IIRI pathogenesis. We examine how these modifications orchestrate multiple signaling cascades, including JAK/STAT, PI3K/Akt, AMPK, and MAPK pathways, by altering protein activity, stability, and interaction networks, thereby influencing cellular survival, apoptotic mechanisms, and inflammatory processes. Looking forward, we anticipate further investigation into the complexity and temporal dynamics of additional PTM types, as well as the interplay between various modifications and their systemic regulatory functions, to better understand PTMs in IIRI pathophysiology and develop novel therapeutic interventions.
Intestinal ischemia-reperfusion injury (IIRI) represents a severe acute abdominal condition characterized by high mortality and multifaceted pathophysiological mechanisms. The principal features include tissue oxygen deficiency during ischemic phases followed by intensified oxidative stress during reperfusion, resulting in intestinal mucosal barrier dysfunction, inflammatory mediator release, and cellular death pathways activation. Recent advances have highlighted the significance of post-translational modifications (PTMs) in regulating protein functionality. This review explores various key PTMs (phosphorylation, acetylation, methylation, ubiquitination, and glycosylation) and their involvement in IIRI pathogenesis. We examine how these modifications orchestrate multiple signaling cascades, including JAK/STAT, PI3K/Akt, AMPK, and MAPK pathways, by altering protein activity, stability, and interaction networks, thereby influencing cellular survival, apoptotic mechanisms, and inflammatory processes. Looking forward, we anticipate further investigation into the complexity and temporal dynamics of additional PTM types, as well as the interplay between various modifications and their systemic regulatory functions, to better understand PTMs in IIRI pathophysiology and develop novel therapeutic interventions.
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