Visomitin attenuates pathological bone loss by reprogramming osteoclast metabolism via STAT3/LDHB axis

A persistently substantial energy demand and metabolic reprogramming endure throughout the entire course of osteoclastogenesis, accompanied by an intensified oxidative stress. Hence, balancing cellular energy metabolism and mataining redox homeostasis offers potential for coordinating osteoclastogenesis and bone loss in pathological conditions. In the present study, we have discovered Visomitin, a novel antioxidant that specifically targets mitochondria, which efficiently decreases intracellular reactive oxygen species levels, inhibits osteoclastogenesis, and impairs bone resorption. Overall design: BMMs were cultured under osteoclastic differentiation conditions for 5 days, either in the presence or absence of Visomitin treatment. Subsequently, the samples were subjected to transcriptome RNA-seq.