Platelet glycoprotein 4 (CD36)

Where the papers sit

9 papers from the last 6 months study Platelet glycoprotein 4 (CD36) directly · updated from PubMed 2 Nov 2026

• CD36 in Steatotic Liver Disease

  CD36 is a central mediator of MASLD, linking hepatocyte lipid uptake with inflammation and fibrosis. Human stem-cell models, 1-naphthol exposure, and steatotic-cell exosomes implicate CD36 through polygenic risk, CA3, and miR-122-5p/ATP6V1H signaling. Endothelial USP12/CD36 activity and macrophage heterogeneity extend the mechanism beyond hepatocytes, while celastrol is proposed as an intervention. The open question is whether blocking CD36 translocation or signaling can halt progression from steatosis to fibrosis.

  5 papers · 55.6%

• Lipid Metabolism and Resistance

  Lipid metabolism is being linked to both gut–liver microbial regulation and therapeutic resistance. Chlorogenic acid shifts Lactobacillus, Ligilactobacillus, and Bacteroides alongside improved lipid handling in hyperlipidemic mice. In cancer, CD276 enhances CD36-mediated lipid metabolism and resistance to tyrosine kinase inhibitors. Whether microbiota-directed metabolic correction can influence CD36-associated drug resistance remains open.

  2 papers · 22.2%

• Others — CD36 in Injury Responses

  Particle exposure is linked to adipogenic and metabolic dysregulation, whereas aloe-emodin engages CD36–PPARγ signaling to clear myelin debris. The shared biology is CD36-dependent handling of lipid or myelin material. Styrene-associated nano- and microplastics emphasize size-specific effects, with membrane depolarization and NFKB1-related signaling among the reported changes. Evidence remains split between toxic metabolic injury and microglial repair, so no single translational direction emerges.

  2 papers · 22.2%