ArticleEMBO molecular medicine2025
Mitochondrial damage drives T-cell immunometabolic paralysis after major surgery.
Article in EMBO molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Prognostic Nutritional Index as a Predictor of 90-Day Mortality in Surgical Sepsis Patients with Acute Kidney Injury-A Retrospective Cohort Study Based on the MIMIC-IV Database.Journal of clinical medicine · 2026Article
- IL-18 derived from microwave-ablated osteosarcoma facilitates antitumor response.Journal for immunotherapy of cancer · 2026Article
- Current concepts on feeding the critically ill patient: a narrative review.Critical care (London, England) · 2026Review
- Immunometabolism in Cardiac Remodeling: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Gene expression changes in lymphocytes and monocytes from patients with traumatic brain injury.Scientific reports · 2026Article
- Mitochondrial unfolded protein response as a central stress-integration hub: mechanisms and implications in disease contexts.Burns & trauma · 2026Review
- Mitochondrial dysfunction in immune cells during the perioperative period: mechanisms, emerging therapeutic strategies, and implications for multi-organ protection.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
27 authors.
Funding
Abstract
Cytotoxic T cell (CTL) dysfunction is a hallmark of immune paralysis after major surgery, increasing susceptibility to severe nosocomial infections and contributing to mortality in critically ill patients. The mechanisms remain poorly understood. We demonstrate that reactive oxygen species (ROS) released by myeloid-derived suppressor cells (MDSC) transiently emerging after surgery, drive perioperative CTL immunoparalysis. These ROS damage CTL mitochondria, triggering secondary mitochondrial ROS amplification and overwhelming antioxidant defenses. The resulting oxidative cascade impairs oxidative phosphorylation and suppresses CTL effector function. Concurrently, stress-induced mitochondrial hyperfusion disrupts fission-dependent translocation to the immunological synapse, exacerbating bioenergetic failure. MitoTEMPO, a mitochondria-targeted antioxidant, partially mitigates these effects, highlighting mitochondrial stabilization as a potential strategy to prevent perioperative immune dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.