ArticleNature communications2025
Nucleophosmin 1 lactylation in graft kidney induces ferroptotic trigger waves that exacerbate delayed graft function.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The lactate-lactylation axis in acute kidney injury: mechanisms from metabolic reprogramming to epigenetic regulation and clinical therapeutic prospects.International urology and nephrology · 2026Review
- KRAS/ERK2-driven stabilization of AARS1 reprograms tumor metabolism and confers Sorafenib resistance in lung adenocarcinoma.Cell death and differentiation · 2026Article
- Ferroptotic propagation: from single-cell execution to tissue-scale death programs.Cell research · 2026Review
- Lactate-dependent regulation of ferroptosis: redox homeostasis, lactylation, and translational perspectives.Apoptosis : an international journal on programmed cell death · 2026Review
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Lactylation-regulated ferroptosis: mechanisms, disease associations, and therapeutic strategies.Archives of pharmacal research · 2026Review
- Lactylation in kidney diseases: a review of regulatory mechanisms and therapeutic prospects.Frontiers in cell and developmental biology · 2026Review
- Nucleophosmin 1 proteins as potential therapeutic targets in non-communicable chronic inflammatory diseases: a review of pathophysiological mechanisms.Frontiers in cell and developmental biology · 2026Review
- Protective Effect of Salidroside Against Multiple Organs Ischemia-Reperfusion Injury: New Insights From Common and Specific Pharmacological Mechanisms.Drug design, development and therapy · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Ferroptotic waves aggravate kidney ischemia-reperfusion injury and drive delayed graft function (DGF). We demonstrate that elevated glycolysis and lactate production in graft kidney correlate with ferroptosis and functional impairment. A signaling axis composed of the long non-coding RNA IGIP-5, microRNA 670-3p, and lactate dehydrogenase A promotes lactate secretion from injured tubular cells, inducing lactylation and ferroptosis in neighboring cells and triggering ferroptotic waves. Lactylome profiling identifies that nucleophosmin 1 (NPM1), an epigenetic regulator, is lactylated at lysine 257 by the lactyltransferase AARS1. Suppressing NPM1 lactylation-via K257 mutation, AARS1 knockout, or taurochenodeoxycholic acid-upregulates SLC7A11 and inhibits ferroptosis. Mechanistically, lactylation stabilizes NPM1 by reducing MDM2-mediated ubiquitination and strengthens SLC7A11 repression, disrupting cystine metabolism. In mouse allografts, blocking lactate shuttle-mediated NPM1 lactylation prevents ferroptotic propagation and ameliorates graft function. Additionally, we develop an early prediction model for DGF using postoperative urinary lactate concentrations. These findings reveal a metabolic-epigenetic axis driving ferroptotic propagation and propose NPM1 lactylation as a therapeutic target for DGF.
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Registered trials
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