ArticleJHEP reports : innovation in hepatology2026
CD36-PPARγ-SPP1 axis mediates hepatocyte-macrophage coordination to drive MASLD-related liver fibrosis.
Article in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Fucoxanthin Suppresses Lipid Accumulation and Inflammatory Responses in FFA-Induced Hepatocyte Models via the EGR2-CD36 Axis.Molecules (Basel, Switzerland) · 2026Article
- GSTM3 Knockdown Promotes Liver Fibrosis Reversal by Inhibiting Hepatic Stellate Cell Activation via PPARγ Signaling.Journal of clinical and translational hepatology · 2026Article
- Macrophages in MASLD: from inflammatory and metabolic crosstalk to exercise intervention.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background & Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by profound remodeling of hepatic macrophages, including the emergence of lipid-associated macrophages (LAMs). However, the mechanisms through which LAMs promote fibrosis and their key molecular drivers remain elusive. Methods: Macrophage-specific CD36 knockdown was achieved using AAV8-delivered short hairpin (sh)RNA. A suite of experimental systems, including co-culture models, lipid trafficking assays, chromatin immunoprecipitation sequencing (ChIP)-qPCR, and lipidomics, was used to dissect the cluster of differentiation (CD)36-peroxisome proliferator-activated receptor (PPAR)γ-SPP1 axis. Genetic and pharmacological tools were used for mechanistic and therapeutic studies. Clinical relevance was assessed in well-characterized patient cohorts. Results: We identified a unique CD36 Conclusions: Our study identifies the CD36-PPARγ-SPP1 axis as a core mechanism whereby lipid-loaded macrophages drive liver fibrosis in MASLD. Thus, therapeutic cotargeting of CD36 and PPARγ presents a novel and promising strategy to counteract fibrosis progression in advanced disease. Impact and implications: Our study provides an investigation of the features and signals of lipid-associated macrophages (LAMs) that are present in MASLD liver and express a specific protein called CD36. We found that these cells internalize hepatocyte-derived lipids via CD36 and activate the PPARγ-SPP1 axis, contributing to liver fibrosis. More importantly, targeting CD36 effectively improves serum aminotransferases, liver steatosis, and liver fibrosis. Understanding the novel signal in LAMs and discovering the diverse roles of PPARγ in different cell populations could be therapeutically targeted to treat MASLD-related liver fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.