{
  "abstract": "Glioblastoma (GBM) is one of the most aggressive primary malignant tumors in the central nervous system. It is characterized by significant metabolic reprogramming, obvious glycolysis dependence, and excessive lactate accumulation. Rather than being merely a metabolic by-product, lactate is increasingly recognized as a signaling metabolite that can reshape tumor biology. The discovery of lactylation as a post-translational modification has established a direct mechanistic link between lactate metabolism, epigenetic regulation, and protein function. Evidence from GBM and broader glioma models indicates that lactylation regulates various carcinogenic processes, including tumor cell proliferation, maintenance of stemness, DNA damage repair, immune evasion, and resistance to chemotherapy and radiotherapy. Through these processes, lactylation couples metabolic states to transcriptional and signaling networks, thereby promoting malignant progression and treatment failure. This review summarizes current understanding of the molecular mechanisms regulating lactylation and systematically explores its role in the progression of GBM, treatment resistance, and remodeling of the tumor immune microenvironment. We also assess emerging strategies targeting lactate and the main obstacles in its clinical translation. Overall, lactylation may serve as an important regulatory interface connecting metabolic reprogramming and the malignant phenotype of GBM; however, its value as a clinical biomarker or therapeutic target still requires further validation.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Neurosurgery, Affiliated Hospital of Nantong University , ,"
  ],
  "article_type": "review article",
  "arxiv": null,
  "author_total": 4,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Long Huang"
    },
    {
      "affs": [
        0
      ],
      "name": "Boyu Huang"
    },
    {
      "affs": [
        0
      ],
      "name": "Shizhen Kuang"
    },
    {
      "affs": [
        0
      ],
      "name": "Yaohua Yan"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/1z7zn4tncv63g.bib",
  "cited_by": 0,
  "doi": "10.3389/fcell.2026.1940871",
  "fulltext_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13728161/?tool=EBI",
  "id": "1z7zn4tncv63g",
  "issns": [
    "2296-634X"
  ],
  "landing_url": "https://europepmc.org/article/PMC/PMC13728161",
  "language": "eng",
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Review"
    ],
    [
      "openalex",
      "1306|Cancer, Hypoxia, and Metabolism"
    ]
  ],
  "openalex": "W7223049294",
  "pdf_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13728161/pdf/?tool=EBI",
  "pmcid": "PMC13728161",
  "pmid": "42978985",
  "published": "2026-10-20",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/1z7zn4tncv63g.ris",
  "sources": [
    {
      "first_seen": "2026-11-04T15:20:46Z",
      "native_id": "PMC:PMC13728161",
      "source": "europepmc",
      "url": "https://europepmc.org/article/PMC/PMC13728161"
    },
    {
      "first_seen": "2026-11-06T12:23:53Z",
      "native_id": "PMC13728161",
      "source": "pmc",
      "url": "https://doi.org/10.3389/fcell.2026.1940871"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:1306|Cancer, Hypoxia, and Metabolism",
      "subfield": "oncology"
    }
  ],
  "title": "Lactylation in glioblastoma: mechanisms and therapeutic perspectives",
  "title_text": "Lactylation in glioblastoma: mechanisms and therapeutic perspectives",
  "type": "peer-reviewed",
  "updated_at": "2026-11-07T12:21:12Z",
  "url": "https://research.draconitic.com/paper/1z7zn4tncv63g",
  "venue": "Frontiers in cell and developmental biology",
  "versions": []
}