ArticleSmart medicine2024
Roles of Akirin1 in early prediction and treatment of graft kidney ischemia‒reperfusion injury.
Article in Smart medicine, 2024. 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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8 citing papers in PubMed.
- Boosting ribosomal translationBioactive materials · 2026Article
- Exosomes in organ transplantation: roles in immunomodulation, ferroptosis and mitophagy.Frontiers in immunology · 2026Review
- Nucleophosmin 1 lactylation in graft kidney induces ferroptotic trigger waves that exacerbate delayed graft function.Nature communications · 2025Article
- Magnetically navigated nano-PROTAC ameliorates acute lung injury.Journal of nanobiotechnology · 2025Article
- Expression of urinary exosomal miR-136-5p in diabetic kidney disease and evaluation of its clinical diagnostic value.Scientific reports · 2025Article
- Combinational Analysis of Metabolomic and O-GlcNAcylation Omics Reveals the HBP Metabolic Regulation of Chemoresistance via GFPT1/NR3C1 O-GlcNAcylation/GPX4 Axis.Research (Washington, D.C.) · 2025Article
- ProPept-MT: A Multi-Task Learning Model for Peptide Feature Prediction.International journal of molecular sciences · 2024Article
- Roles of Akirin1 in early prediction and treatment of graft kidney ischemia‒reperfusion injury.Smart medicine · 2024Article
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Authors and funding
17 authors.
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Abstract
Ferroptosis is a predominant contributor to graft kidney ischemia‒reperfusion injury (IRI), resulting in delayed graft function (DGF). However, much less is known about the early predicting biomarkers and therapeutic targets of DGF, especially aiming at ferroptosis. Here, we propose a precise predicting model for DGF, relying on the Akirin1 level in extracellular vesicles (EVs) derived from recipient urine 48 h after kidney transplant. In addition, we decipher a new molecular mechanism whereby Akirin1 induces ferroptosis by strengthening TP53-mediated suppression of SLC7A11 during the graft kidney IRI process, that is, Akirin1 activates the EGR1/TP53 axis and inhibits MDM2-mediated TP53 ubiquitination, accordingly upregulating TP53 in two ways. Meanwhile, we present the first evidence that miR-136-5p enriched in EVs secreted by human umbilical cord mesenchymal stem cells (UM-EVs) confers robust protection against ferroptosis and graft kidney IRI by targeted inhibition of Akirin1 but knockout of miR-136-5p in UM sharply mitigates the protection of UM-EVs. The functional and mechanistic regulation of Akirin1 is further corroborated in an allograft kidney transplant model in wild-type and Akirin1-knockout mice. In summary, these findings suggest that Akirin1, which prominently induces ferroptosis, is a pivotal biomarker and target for early diagnosis and treatment of graft kidney IRI and DGF after kidney transplant.
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