ArticleJournal of orthopaedic translation2026
Histone H3K18 lactylation: An exercise-induced epigenetic mechanism that inhibits osteoclast activity and protects against osteoporosis.
Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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18 authors.
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Abstract
Objective: Osteoclasts, through their excessive production, are the primary cause of postmenopausal osteoporosis. However, the influence of metabolism on osteoclastogenesis remains poorly understood. This study reveals that protein lactylation plays a critical role in osteoclast differentiation. Methods: The ovariectomized (OVX) mouse model was used to investigate osteoporosis by examining glycolysis and lactate levels during osteoclast differentiation. Bone resorption was assessed through histomorphometric analysis. The effects of elevating lactate levels were tested both endogenously via exercise and exogenously through sodium lactate (NaLac) administration. Protein lactylation, focusing on histone modifications, was analyzed, and key osteoclastogenesis genes, including cathepsin K ( Results: Our findings showed that glycolysis and lactate levels were reduced during osteoclast differentiation in the OVX model, despite increased bone resorption. Elevating lactate through exercise or sodium lactate supplementation increased protein lactylation and mitigated OVX-induced bone loss. Mechanistically, lactate enhanced histone H3 lysine-18 lactylation (H3K18la), which suppressed osteoclast differentiation by downregulating key osteoclastogenesis genes like Conclusions: Lactate suppresses osteoclast differentiation and alleviates osteoporosis through histone H3K18 lactylation, which downregulates osteoclastogenic genes including The translational potential of this article: This study reveals an epigenetic mechanism by which lactate regulates osteoclast function and suggests that exercise-induced lactate elevation or lactate supplementation may represent a viable therapeutic strategy for postmenopausal osteoporosis.
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