ArticleClinical science (London, England : 1979)2025
Osteoclast-derived exosomal miR-30a-3p promotes lead exposure-induced osteoporosis by triggering osteoblastic pyroptosis.
Article in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- Exosomes in Metabolic Bone Diseases: Regulators, Biomarkers and Targeted Delivery Systems.Biomedicines · 2026Review
- Cold exposure-induced loss of beneficial gut bacterial sEV is associated with the pathogenesis of bone loss through pyroptosis pathway.Journal of nanobiotechnology · 2026Article
- Programmed cell death in degenerative skeletal diseases: molecular crosstalk and combinatorial therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Advances in Injectable miRNA-Loaded Nanocomposite Hydrogel Systems for Cartilage Repair in KOA.International journal of nanomedicine · 2026Review
- Osteoclast-derived exosomes promote medication-related osteonecrosis of the jaw by delivering glycoRNA to disrupt the blood-lymphatic vascular network.Journal of dental sciences · 2026Article
- The recent progression of extracellular vesicles application in osteoporosis.Frontiers in pharmacology · 2026Review
- NLRP3 Inflammasome-Mediated Pyroptosis in Osteoporosis: Osteoimmune Mechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2025Review
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Authors and funding
14 authors.
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Abstract
High lead (Pb) burden in humans disrupts bone homeostasis and can induce osteoporosis. Here, we report that osteoclast-derived exosomes (OC-Exos) were enriched in the plasma of patients with low bone mineral density and Pb exposure. Osteoclasts (OCs) secrete microRNA-enriched exosomes, through which miR-30a-3p is transferred to osteoblasts (OBs) to induce pyroptosis, leading to the aggravation of bone loss. Mechanistically, OC-Exo-packaged miR-30a-3p triggered pyroptosis in OBs by stimulating the NLRP3 inflammasome, activating the caspase-1 pathway, and up-regulating the expression of IL-1 and IL-18. Depletion of miR-30a-3p abolished the effects of OC-Exo and alleviated the symptoms of Pb-induced osteoporosis. Collectively, our results suggest that miR-30a-3p is highly expressed in exosomes derived from OCs and mediates OB pyroptosis, inhibiting bone formation through cellular communication in Pb-induced osteoporosis. Therefore, OC-Exo-packaged miR-30a-3p may be a novel risk factor for Pb-induced osteoporosis and holds prognostic value in evaluating bone formation.
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