ArticleCell death discovery2025
Aging aggravated liver ischemia and reperfusion injury by promoting oxidized mtDNA mediated-macrophage pyroptosis through acetylated MCU-dependent calcium uptake.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- CO-mediated restoration of mitochondrial redox homeostasis contributes to alleviating multiple programmed cell deaths in hepatic I/R injury.Redox biology · 2026Article
- IRF1-mediated sensing of oxidized mitochondrial DNA drives macrophage PANoptosis in lung ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2026Article
- Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies.Journal of translational medicine · 2026Review
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The shortage of liver donors for liver transplantation is currently an urgent problem. Elderly donors have become an important source of donor livers, but they are more prone to ischemia reperfusion injury (IRI) in liver transplantation. Therefore, exploring the effects and mechanisms of aging on liver IRI will provide a new theoretical basis for improving the survival rate of liver transplant patients. We constructed a mouse model of liver ischemia for 90 min and reperfusion for 6 or 24 h, and found that compared with young liver, the recovery of liver function in aged liver after IRI was slower. Detection of macrophage pyroptosis revealed that it was an important factor for aging deferring liver function restoration. Mechanistically, we demonstrated that aging triggered mitochondrial permeability transition pore (mPTP) channel opening to promote the release of Oxidized mtDNA (Ox-mtDNA), thereby inducing macrophage pyroptosis. Moreover, the activity of mPTP channel was mainly dependent on calcium uptake by acetylated mitochondrial calcium uniporter (MCU). These results illustrated that cytoplasmic Ox-mtDNA-induced macrophage pyroptosis was a key factor for aging exacerbating liver IRI. Calcium uptake via acetylated MCU triggered mPTP channel opening, which is an important mechanism for Ox-mtDNA release from mitochondria into the cytoplasm.
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Registered trials
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