ArticleJournal of orthopaedic surgery and research2025
The effect of lactate dehydrogenase B and its mediated histone lactylation on chondrocyte ferroptosis during osteoarthritis.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Protein acylation and bone metabolism: bidirectional crosstalk linking metabolic reprogramming to skeletal homeostasis.Journal of molecular histology · 2026Review
- Lactate-dependent regulation of ferroptosis: redox homeostasis, lactylation, and translational perspectives.Apoptosis : an international journal on programmed cell death · 2026Review
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- Histone lactylation: a novel epigenetic bridge linking cellular metabolism to benign and malignant gynecological diseases.Clinical epigenetics · 2026Review
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Lactylation-regulated ferroptosis: mechanisms, disease associations, and therapeutic strategies.Archives of pharmacal research · 2026Review
- Review
- Lactate and Acidification: Emerging Metabolic Regulators of Osteoarthritis.Current medical science · 2026Review
- Lactylation‑mediated ferroptosis: A novel mechanism and therapeutic prospects in human diseases (Review).International journal of molecular medicine · 2026Review
- [Research progress on lactylation modification in pathogenesis of osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Review
- Research progress on the mechanism of chondrocyte ferroptosis in osteoarthritis.Frontiers in immunology · 2026Review
- Histone lactylation-mediated glycolysis-ferroptosis axis in neurological diseases.Frontiers in molecular neuroscience · 2026Review
- Epigenetic regulation in osteoarthritis: recent updates and emerging mechanisms.Frontiers in genetics · 2026Review
- Lactate-driven lactylation reprograms chondrocyte fate and joint inflammation in osteoarthritis: linking metabolism with epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
- Investigating the Mechanistic Link Between Lactate-Induced Histone Lactylation and Cellular Senescence in Osteoarthritis Chondrocytes: Implications for Therapy.International journal of biological sciences · 2026Article
- Lactylation at the crossroads of immune metabolism and epigenetic regulation: revealing its role in rheumatic immune diseases.Journal of translational medicine · 2025Review
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Roles of lactylation in lipid metabolism and related diseases.Cell death discovery · 2025Review
- Ferroptosis and bone health: bridging the gap between mechanisms and therapy.Frontiers in immunology · 2025Review
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5 authors.
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Abstract
backgroundHistone lactylation is a novel epigenetic regulator that is reported to participate in gene expression. Ferroptosis is an oxidative form of cell death and chondrocyte ferroptosis crucially impacts the development of osteoarthritis (OA). The study aimed at investigating the effect of lactate dehydrogenase B (LDHB) and its mediated histone lactylation on chondrocyte ferroptosis during OA.
methodsOur study focused on the establishment of in vivo mouse model and in vitro interleukin-1β (IL-1β)-induced chondrocytes model and administrated LDHB knockdown (siLDHB). Histopathological assessment of cartilage was conducted via HE staining, while serum levels of cartilage oligomeric matrix protein (COMP) and crosslinked C-telopeptides of type II collagen (CTX-II) were quantified using ELISA to evaluate OA severity. The matrix degradation was further examined by expression of Collagen II and Aggrecan. Levels of total iron, ferrous iron (Fe2+), and lipid reactive oxygen species (ROS) were considered measurements of ferroptosis. Assessment of cell viability and proliferation relied on cell counting kit 8 (CCK-8) together with colony formation assay. Western blotting assay served for detecting the relative expression of proteins and protein lactylation. The epigenetic regulation of ACSL4 by LDHB was determined by chromatin immunoprecipitation (ChIP) and luciferase reporter gene assay.
resultsOA mice presented remarkably elevated protein level of LDHB and H3K18 lactylation in the cartilage versus the sham group. Knockdown of LDHB downregulated the levels of COMP and CTX-II, as well as alleviated chondrocyte ferroptosis in vitro and in vivo. Results from ChIP and luciferase reporter gene assay demonstrated direct histone lactylation of ACSL promoter, and knockdown of LDHB and treatment with LDH inhibitor reduced histone lactylation and expression of ACSL4. ACSL4 overexpression could reverse the impact of LDHB depletion on chondrocyte proliferation and ferroptosis.
conclusionLDHB promotes ACSL4 by histone lactylation to induce chondrocyte ferroptosis, which further contributes to OA development. The findings in the study assist in understanding the modulating mechanism of LDHB-mediated lactylation against chondrocyte ferroptosis in OA progression.
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