Loading
Life sciences · Journal article
Cureus · September 25, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
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.