Mitochondrial Proteomics Uncovers that Myeloid S100A9 Deficiency Promotes Liver Injury and Fibrosis Regression via Mitochondrial Metabolic Reprogramming of Macrophages.

Key Points

• This research aims to explore the role of S100A9 in macrophage metabolism and its impact on liver fibrosis.
• Utilized a mouse model to assess the effects of genetic deletion of S100A9 in myeloid cells.
• Examined changes in macrophage subtypes, particularly CD206-positive M2-like macrophages, during liver fibrosis.
• Analyzed mitochondrial metabolic activity in macrophages during liver injury.
• S100A9-deficient macrophages were found to reduce liver injury and fibrogenesis.
• Increased proportions of CD206-positive M2-like macrophages were associated with S100A9 deficiency, indicating a shift toward an anti-inflammatory response.
• Targeting macrophage S100A9 presents potential as a therapeutic strategy against liver fibrosis.