ArticleJHEP reports : innovation in hepatology2025
Macrophage MRC2 deficiency mitigates HFD-induced MASLD by downregulating CD147-regulated TNF-α production.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Targeting macrophage metabolism: mechanisms, cellular crosstalk and implications in obesity-associated metabolic diseases.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Background & Aims: The mechanisms underlying metabolic dysfunction-associated steatotic liver disease (MASLD) remain incompletely understood, and macrophage-associated chronic inflammation has been suggested to play a role. We investigated the potential contribution of mannose receptor type C 2 (MRC2), a transmembrane glycoprotein, to MASLD development. Methods: Wild-type (WT) and Results: MRC2 levels were significantly elevated in patients with MASLD (n = 216, Conclusions: Macrophage MRC2 promotes HFD-induced hepatic steatosis via the MRC2-CD147 complex, revealing a novel mechanism contributing to MASLD progression. Impact and implications: This study identifies the critical role of MRC2 in the development of high-fat diet-induced metabolic dysfunction-associated steatotic liver disease, providing a mechanistic understanding of its involvement in macrophage-mediated inflammation.
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