ReviewFrontiers in endocrinology2025
Lactylation in diabetes mellitus and its complications: mechanisms of action and therapeutic potential - recent advances.
Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Subclinical Atherosclerosis, Hyperlipidemia and New-Onset Diabetes Should Not Be Ignored Despite Initial Angiographic Exclusion of Significant Atherosclerotic Occlusive Arterial Disease.Diagnostics (Basel, Switzerland) · 2026Article
- Unveiling lactylation: A novel frontier in the pathogenesis of diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- From Byproduct to Regulator: The Expanding Role of Lactate and Lactylation in Cardiovascular Physiology and Disease.Biology · 2026Review
- Lactylation: a metabolic-epigenetic bridge in diabetic kidney disease and a therapeutic target for TCM.Chinese medicine · 2026Review
- Lactate Metabolism and Protein Lactylation in Diabetic Kidney Disease: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Diabetes mellitus (DM) and its complications represent a global health burden. Lactylation, a novel post-translational modification (PTM) linking metabolism to epigenetic regulation, has emerged as a key mediator in metabolic disorders. Objective: This review systematically summarizes the regulatory roles and therapeutic potential of lactylation in DM pathogenesis and complications. Key Findings: (1) Lactylation modulates core diabetic pathways by targeting IRS-1 (promoting insulin resistance), NLRP3 (amplifying inflammation), and FOXO1 (enhance oxidative stress); (2) Tissue-specific regulation is observed in complications: lactylation of LARS1 and ACSF2 exacerbates podocyte injury and mitochondrial dysfunction in nephropathy; the FTO-CDK2 axis drives vascular anomalies in retinopathy; and H4K12 lactylation activates Foxo1-mediated oxidative stress in cognitive impairment. Conclusion: Lactylation functions as a critical metabolic-epigenetic hub, and targeting its "writer-eraser-reader" system may offer novel therapeutic strategies for DM and complications, requiring further clinical translation.
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Registered trials
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