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

-deficient macrophages. Finally, we found that genetic deletion of S100A9 in myeloid cells protected against liver injury and fibrogenesis through increasing the proportion of hepatic CD206-positive M2-like anti-inflammatory macrophages in a mouse model. Our study uncovers a novel role of S100A9 in macrophage mitochondrial metabolism and phenotype reprogramming during liver fibrosis, and targeting macrophage S100A9 may be considered as a potential therapeutic strategy against liver fibrosis.