{
  "abstract": "Histone H3 lysine 18 lactylation (H3K18la) links fluctuations in lactate metabolism with chromatin-dependent transcription. Promoter- and enhancer-level associations suggest that H3K18la can report local metabolic-chromatin coupling, but evidence for modification-specific causality remains uneven because the known writers and erasers are promiscuous, dedicated readers are poorly defined, and broad acyltransferase inhibitors perturb competing histone and non-histone marks. Across tumor, inflammatory, metabolic, cardiovascular, and degenerative-disease models, H3K18la participates in oncogenic, immunoregulatory, fibrotic, or reparative programs according to cell lineage, chromatin state, metabolic exposure, and disease stage. We synthesize these observations using a testable framework in which lactate and lactyl-CoA provide metabolic permission, whereas transcription factors, chromatin accessibility, histone chaperones, and candidate protein or RNA scaffolds provide locus selection; downstream readers or conventional transcriptional effectors then shape the biological output. Direct long non-coding RNA (lncRNA)-guided deposition and a universally validated H3K18la reader remain unproven. Human cohort data support exploratory, disease-specific associations, but assay heterogeneity and the lack of prospective external validation preclude current clinical use. Progress will require histone H3 lysine 18 acetylation (H3K18ac)-aware, inhibitor-independent causal tests, structural validation of readers, integrated chromatin-RNA profiling, and prospective multicenter cohorts.",
  "abstract_shown": true,
  "affiliations": [
    "epartment of Pathology, Affiliated Hospital of Nantong University, Nantong, China"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Ting Wu"
    },
    {
      "affs": [
        0
      ],
      "name": "Yali Zhang"
    },
    {
      "affs": [
        0
      ],
      "name": "Yifei Liu"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/7efndy9s7n3py.bib",
  "cited_by": 0,
  "doi": "10.3389/fgene.2026.1950620",
  "fulltext_url": "https://www.frontiersin.org/articles/10.3389/fgene.2026.1950620/full",
  "id": "7efndy9s7n3py",
  "issns": [
    "1664-8021"
  ],
  "landing_url": "https://doi.org/10.3389/fgene.2026.1950620",
  "language": "en",
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "lcc",
      "QH426-470"
    ],
    [
      "openalex",
      "1312|Genomics and Chromatin Dynamics"
    ]
  ],
  "openalex": "W7223565676",
  "pdf_url": "https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2026.1950620/pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-26",
  "publisher": "Frontiers Media S.A.",
  "ris": "https://research.draconitic.com/paper/7efndy9s7n3py.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T13:47:13Z",
      "native_id": "63a7103dea5d4cc3b327a1a282125cf3",
      "source": "doaj",
      "url": "https://doi.org/10.3389/fgene.2026.1950620"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "openalex:1312|Genomics and Chromatin Dynamics",
      "subfield": "molecular-biology"
    }
  ],
  "title": "Divergent roles of H3K18 lactylation in human diseases: metabolic-epigenetic circuits and translational challenges",
  "title_text": "Divergent roles of H3K18 lactylation in human diseases: metabolic-epigenetic circuits and translational challenges",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T13:47:13Z",
  "url": "https://research.draconitic.com/paper/7efndy9s7n3py",
  "venue": "Frontiers in Genetics",
  "versions": []
}