{
  "abstract": "Hepatocellular carcinoma (HCC) is a leading cause of cancer death and is associated with metabolic dysfunction and chronic liver disease. Lipid metabolic reprogramming is a key hallmark of HCC, and CD36, a fatty acid translocase and scavenger receptor, has emerged as a central regulator of this process. This review investigated the multifaceted roles of CD36 in HCC pathogenesis. CD36 facilitates long-chain fatty acid uptake and affects oncogenic signaling and the tumor immune microenvironment. CD36-mediated lipid accumulation promotes cytotoxic T-cell function and macrophage M2 polarization and drives immune evasion. Likewise, CD36 modulates ferroptosis sensitivity by influencing polyunsaturated fatty acid-induced lipid peroxidation and redox balance. Through metabolic plasticity and oxidative stress adaptation, CD36 also contributes to resistance to chemotherapy, targeted therapies, and immunotherapy. In conclusion, CD36 serves as a critical multifunctional regulator linking lipid metabolism, ferroptosis, immunomodulation, and therapy resistance in HCC, positioning it as a promising therapeutic target for improving clinical outcomes. However, clinical translation remains challenging due to the broad tissue expression of CD36 and the lack of large-scale clinical validation. Hence, future research should focus on clinical validation of CD36, mechanistic elucidation, selective inhibitor development, combination therapy evaluation, and multi-omics-guided personalized HCC treatment.",
  "abstract_shown": true,
  "affiliations": [
    "Department of General Surgery, Yangzhou University, Yangzhou, CHN.",
    "Department of General Surgery, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, CHN."
  ],
  "article_type": "review article",
  "arxiv": null,
  "author_total": 2,
  "authors": [
    {
      "affs": [
        0,
        1
      ],
      "name": "Ankit Kumar Bijaraniya"
    },
    {
      "affs": [
        1
      ],
      "name": "Tao Lide"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/cmtr70cevemjk.bib",
  "cited_by": 0,
  "doi": "10.7759/cureus.116886",
  "fulltext_url": "https://europepmc.org/articles/PMC13695763",
  "id": "cmtr70cevemjk",
  "issns": [
    "2168-8184"
  ],
  "landing_url": "https://europepmc.org/article/MED/42928736",
  "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": [
    [
      "openalex",
      "1306|Cancer, Lipids, and Metabolism"
    ]
  ],
  "openalex": "W7214302316",
  "pdf_url": "https://europepmc.org/articles/PMC13695763?pdf=render",
  "pmcid": "PMC13695763",
  "pmid": "42928736",
  "published": "2026-09-25",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/cmtr70cevemjk.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:21:18Z",
      "native_id": "MED:42928736",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/42928736"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:1306|Cancer, Lipids, and Metabolism",
      "subfield": "oncology"
    }
  ],
  "title": "CD36-Mediated Lipid Metabolic Reprogramming in Hepatocellular Carcinoma: Crosstalk With Immunity, Ferroptosis, and Therapeutic Resistance.",
  "title_text": "CD36-Mediated Lipid Metabolic Reprogramming in Hepatocellular Carcinoma: Crosstalk With Immunity, Ferroptosis, and Therapeutic Resistance.",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:21:18Z",
  "url": "https://research.draconitic.com/paper/cmtr70cevemjk",
  "venue": "Cureus",
  "versions": []
}