Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies
Shen R., An P., Chen M., Lu P., Yang J., Wu L.
Narrative Review, published in J Transl Med (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- J Transl Med (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41998683
- PMCID
- PMC13217771
- DOI
- 10.1186/s12967-026-08155-5
Abstract (original English)
BACKGROUND: Hepatic ischemia-reperfusion injury (IRI) is a common pathological process in liver surgery, which seriously affects the prognosis of patients. Its core mechanism is closely related to a vicious cycle triggered by an imbalance in mitochondrial quality control and abnormal release of mitochondrial DNA (mtDNA). MAIN BODY: When mitochondria are damaged by ischemia and hypoxia, dysfunction in key quality control processes—including mitochondrial autophagy, which clears damaged components, mitochondrial dynamics (fusion/fission) that regulate morphology, and the formation of mitochondrial-derived vesicles (MDVs)—prevents the effective isolation or elimination of damage. This leads to increased mitochondrial membrane permeability, facilitating the release of mtDNA into the cytoplasm. Released mtDNA serves as a key signaling molecule that directly drives various forms of programmed cell death. It promotes apoptosis by activating the cGAS-STING pathway. As a damage-associated molecular pattern (DAMP), it can also trigger NLRP3 inflammasome-mediated and GSDMD-mediated pyroptosis. Additionally, it promotes ferroptosis by amplifying oxidative stress and disrupting iron metabolism. Ultimately, mtDNA aggravates uncontrolled innate immune responses and cell death through inflammatory pathways like cGAS-STING, NLRP3, and TLR9, further amplifying tissue injury. Therefore, preventin
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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