ArticleInternational journal of biological sciences2025
SIRT4-Mediated Deacetylation of PRDX3 Attenuates Liver Ischemia Reperfusion Injury by Suppressing Ferroptosis.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Cell death in ischemia-reperfusion injury: beyond a single-cell-death perspective.Biomarker research · 2026Review
- [SingleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- The Mechanism of G Protein-Coupled Receptor Regulation of Ferroptosis in Hepatic Ischemia-Reperfusion Injury.International journal of molecular sciences · 2026Review
- SIRT4 regulates antiviral and autoimmune responses by promoting cGAS-mediated signaling pathways.EMBO reports · 2026Article
- The role of lysine acylation in metabolic dysregulation and inflammatory responses within the hepatic immune microenvironment of MASLD.Frontiers in immunology · 2026Review
- Sirtuin 4 Knockout Aggravates Sepsis-Induced Acute Liver Injury by Enhancing Mitochondrial Fission and Mitophagy in Hepatocytes.Mediators of inflammation · 2026Article
- Hypoglycemia aggravates cognitive degeneration by activating endothelial ZBP1-mediated PANoptosis in type 2 diabetic mice.Frontiers in pharmacology · 2026Article
- Nanomedicine in Organ Transplantation: From Graft Preservation and Repair to Immunomodulation and Monitoring.Theranostics · 2026Review
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver ischemia-reperfusion injury (LIRI) is an important cause of the clinical prognosis of liver transplantation. Despite Sirtuin 4 (SIRT4) is involved in various post-translational modifications, its role in LIRI is unclear. This research aimed to investigate the influence of SIRT4 on the pathogenesis of LIRI. To this end, SIRT4 knockout (KO) and liver-specific overexpression mice, as well as alpha mouse liver 12 (AML12) cells, were employed. We showed that SIRT4 expression was downregulated in mice with LIRI or AML12 cells exposed to hypoxia-reoxygenation (H/R) injury, as well as in the liver tissue of liver transplant patients. SIRT4 KO exacerbated liver injury and ferroptosis; conversely, liver-specific SIRT4 overexpression in mice produced the opposite results. Furthermore, the ferroptosis inhibitor ferrostatin-1 mitigated the exacerbation of liver injury and ferroptosis caused by SIRT4 KO. Mechanistically, SIRT4 interacted with peroxiredoxins 3 (PRDX3) and deacetylated it at lysine 92, leading to the inhibition of ferroptosis. Furthermore, the protective effect of SIRT4 on LIRI was dependent on PRDX3 deacetylation at lysine 92. Additionally, liver-targeted lipid nanoparticles (LNPs)-sirt4 mRNA alleviated LIRI and ferroptosis in mice. Taken together, our findings highlight the SIRT4-PRDX3 axis as a key regulator and potential therapeutic target for LIRI.
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