ArticleFrontiers in pharmacology2025
Icaritin inhibits osteoclast differentiation and reduces bone loss by targeting ESR1 to inhibit miR503/RANK pathway.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Plant-Based Biomaterials as Bio-Instructive Immunomodulators: Design Principles, Mechanisms, and Translational Challenges.Life (Basel, Switzerland) · 2026Review
- Neferine inhibits vascular smooth muscle cell proliferation and migration in atherosclerosis by targeting CYS130 and PHE252 in PTEN.Frontiers in pharmacology · 2026Article
- Traditional Chinese medicine-derived monomers improve bone metabolic imbalance and delay osteoporosis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
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8 authors.
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Abstract
Background: Postmenopausal osteoporosis (PMOP) is a prevalent metabolic disorder characterized by pathogenic mechanisms associated with the dysfunction of osteoclasts (OC) and osteoblasts (OB). Icaritin (ICT) is a flavonoid derived from icariin and epimedium, which is a natural product, and has demonstrated promising anti-osteoporosis properties. Nevertheless, the targets and mechanisms of ICT in osteoclast differentiation and PMOP remain unclear. Methods: we developed a bilateral ovariectomy-induced osteoporosis model in animals and receptor activator of nuclear factor kappa-B ligand (RANKL) induced RAW264.7 to differentiate into osteoclasts with or without MPP dihydrochloride (MPP) and antagomir-503-5p. Micro-CT, tartrate-resistant acid phosphatase (TRAP) staining, enzyme-linked immunosorbent assay (ELISA), Western blot and qRT-PCR were used to detect bone resorption function, bone metabolism parameters, osteoclast differentiation rate and the expression of related genes, as well as the expression of ESR1, miR-503 and RANK. Molecular docking, cell thermal shift assay (CETSA) and drug affinity responsive target stability (DARTs) experiments were used to confirmed that ESR1 is the direct target of ICT, and binding site of ICT with ESR1. Results: ICT significantly inhibited OC differentiation and the expression of related genes ( Conclusion: Taken together, our study confirmed that ESR1 is the direct target of ICT, and Asparagine at 455 is the direct binding site of ICT, and ICT inhibits OC differentiation and reduces bone loss by targeting ESR1 to upregulate miR503 level and weaken miR503/RANK pathway.
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