Macrophage MRC2 deficiency mitigates HFD-induced MASLD by downregulating CD147-regulated TNF-α production.

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 Mrc 2-deficient mice were fed a high-fat diet (HFD) for 8 weeks. Mouse primary hepatocytes (MPHs) and bone marrow-derived macrophages (BMDMs) were stimulated with or without palmitic acid (PA) to assess the role of MRC2 in MASLD development.

Results

MRC2 levels were significantly elevated in patients with MASLD (n = 216, p <0.0001) and in the livers of HFD-fed WT mice (n =

SUBMITTER: Kuo HR 

PROVIDER: S-EPMC12682121 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature