ArticleHepatology communications2024
The cell fate regulator DACH1 modulates ferroptosis through affecting P53/SLC25A37 signaling in fibrotic disease.
Article in Hepatology communications, 2024. 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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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting Ferroptosis With Natural Products for the Treatment of Skeletal System Disease: An Updated Review.Journal of cellular and molecular medicine · 2026Review
- Identification and validation of NETs-associated biomarkers in osteoporosis with diabetes.Scientific reports · 2026Article
- The cross-talk and interplay between ferroptosis and cuproptosis in tumor and therapeutics.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Scoparone-Induced Phase Separation of ZDHHC12 Drives Ferroptosis via ATG12 S-palmitoylation and Ferritinophagy in Liver Fibrosis.Research (Washington, D.C.) · 2026Article
- Geno-guided targeting of ferroptosis: a multi-layered network to overcome radioresistance in lung cancer.Frontiers in cell and developmental biology · 2026Review
- The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs.Biomolecules · 2025Review
- Unveiling ferroptosis: a new frontier in skin disease research.Frontiers in immunology · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDachshund homolog 1 (DACH1) is widely acknowledged for its involvement in regulating diverse cell fates, but its precise regulatory mechanism in ferroptosis remains elusive. In this study, we investigated whether DACH1 modulates ferroptosis through affecting P53/solute carrier family 25 member 37 (SLC25A37) signaling in hepatic fibrogenesis.
methodsCRISPR-Cas9 system was used to knockout DACH1 in HSC to determine the effect of DACH1 on ferroptosis. Immunoprecipitation, pulldown, and mouse model of hepatic fibrogenesis were used to analyze the potential molecular mechanism of ferroptosis regulation by DACH1.
resultsWe found that ferroptosis inducers increased the protein expression of DACH1 by suppressing the ubiquitin-proteasome signaling. DACH1 knockout can resist ferroptosis, whereas DACH1 knockin can enhance it. Interestingly, the upregulation of DACH1 resulted in the mitochondrial translocation of p53 by inducing phosphorylation at serine 392. The mutation of serine 392 can prevent the combination of DACH1 and p53, the mitochondrial translocation of p53, and DACH1-mediated ferroptosis. Moreover, SLC25A37 was identified as a candidate target for mitochondrial p53. The binding of p53 to SLC25A37 can enhance the iron uptake capacity of SLC25A37, which may cause an overload of iron in the mitochondria and hyperactive mitochondrial electron transport chain. Knockdown of SLC25A37 can impair p53-mediated mitochondrial iron overload and ferroptosis. Furthermore, treatment with erastin can induce HSC ferroptosis and relieve fibrotic lesion damage in the mouse model of hepatic fibrogenesis. HSC-specific knockdown of DACH1, p53, and SLC25A37 can abolish the induction of HSC ferroptosis and reversal of hepatic fibrogenesis by erastin treatment.
conclusionsOur findings suggest that the DACH1/P53/SLC25A37 signaling pathway is a promising target for fibrotic disorders and reveals new regulatory mechanisms of ferroptosis.
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