Mitochondrial Proteomics Uncovers Myeloid S100A9 Deficiency Promotes Liver Injury and Fibrosis Regression via Mitochondrial Metabolic Reprogramming of Macrophages
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ABSTRACT: Macrophage-mediated inflammation has been implicated in the pathogenesis of liver fibrosis. Metabolic reprogramming involves in the transition of macrophages from a pro-inflammatory M1-phenotype toward an anti-inflammatory M2-phenotype. S100A9 is highly expressed in activated macrophages and promotes M1 polarization, however, it is unknown whether S100A9 alters the polarization state of macrophages by regulating metabolism. This study revealed enhanced oxidative phosphorylation (OXPHOS) in S100a9-deficient macrophages based on mitochondrial proteomics, characterized by increased mitochondrial fusion and elevated ATP production.
ORGANISM(S): Mus Musculus
SUBMITTER:
Ping Xu
PROVIDER: PXD070260 | iProX | Mon Nov 03 00:00:00 GMT 2025
REPOSITORIES: iProX
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