An Old Antibiotic’s New Trick: Halting Fibrosis by Targeting Immune Cell Powerhouses
A study published in *Arthritis & Rheumatology* reveals that the antibiotic linezolid, known for targeting bacterial ribosomes, has a potent antifibrotic effect by inhibiting mitochondrial translation in human fibroblasts and macrophages. Researchers demonstrated that linezolid reverses profibrotic gene expression, downregulates key signaling pathways like TGFβ and JAK-STAT, and reduces collagen deposition in models of systemic sclerosis. The mechanism involves disrupting oxidative phosphorylation and glycolysis, metabolic pathways essential for fibroblast activation, thereby preventing tissue fibrosis in skin and lung models.
Why it might matter to you: This research directly connects mitochondrial function in innate immune cells like macrophages and fibroblasts to the pathogenesis of fibrotic diseases, a core topic in immunopathology. For professionals focused on immunology and immunotherapy, it highlights a clinically approved drug with a novel immunomodulatory mechanism, offering a rapid translational pathway for treating autoimmune and fibrotic disorders where current options are limited.
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