ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
NLRP3 mediates osteolysis through inflammation-dependent and -independent mechanisms.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 73 citations in OpenAlex.
- Pyroptotic cell-derived factors promote osteoclast differentiation.bioRxiv : the preprint server for biology · 2026Article
- Non-pyroptotic caspase-11 activity regulates osteoclastogenesis and pathological bone loss.Cell death and differentiation · 2026Article
- Context-dependent roles of the NLRP3 inflammasome in osteomyelitis and strategies for precision modulation.Frontiers in immunology · 2026Review
- Naringin inhibits the osteoblast-osteoclast pyroptosis cascade reaction mediated by accumulated bone marrow adipose tissue in the treatment of postmenopausal osteoporosis.Journal of orthopaedic translation · 2025Article
- Topography-based implants for bone regeneration: Design, biological mechanism, and therapeutics.Materials today. Bio · 2025Review
- Pyroptosis: A spoiler of peaceful coexistence between cells in degenerative bone and joint diseases.Journal of advanced research · 2025Review
- DAMPs, PAMPs, NLRs, RIGs, CLRs and TLRs - Understanding the Alphabet Soup in the Context of Bone Biology.Current osteoporosis reports · 2025Review
- Proteases and Osteoporosis: A Comprehensive Review of Their Role in Bone Health.Current drug targets · 2025Review
- Programmed Cell Death in Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Zoledronic Acid Inhibits Lipopolysaccharide-Induced Osteoclastogenesis by Suppressing Macrophage NLRP3-Mediated Autophagy Pathway.Immunity, inflammation and disease · 2024Article
- FDA-approved disulfiram inhibits the NLRP3 inflammasome by regulating NLRP3 palmitoylation.Cell reports · 2024Article
- Article
- The role of autophagy in SIM mediated anti-inflammatory osteoclastogenesis through NLRP3 signaling pathway.Immunity, inflammation and disease · 2024Article
- Pyroptosis mediates osteoporosis via the inflammation immune microenvironment.Frontiers in immunology · 2024Review
- Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.Frontiers in cell and developmental biology · 2024Review
- Pyroptosis -related potential diagnostic biomarkers in steroid-induced osteonecrosis of the femoral head.BMC musculoskeletal disorders · 2023Article
- Pyroptosis in bone loss.Apoptosis : an international journal on programmed cell death · 2023Review
- Effects of NLRP3 on implants placement.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Review
- The regulatory role and therapeutic application of pyroptosis in musculoskeletal diseases.Cell death discovery · 2022Review
- Topography-mediated immunomodulation in osseointegration; Ally or Enemy.Biomaterials · 2022Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Activating-mutations in NOD-like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) cause neonatal-onset multisystem inflammatory disease. However, the ontogeny of skeletal anomalies in this disorder is poorly understood. Mice globally expressing the D301N mutation in Nlrp3 (D303N in human) model the human phenotype, including systemic inflammation and skeletal deformities. To gain insights into the skeletal manifestations, we generated mice in which the expression of D301N Nlrp3 (Nlrp3( D301N)) is restricted to myeloid cells. These mice exhibit systemic inflammation and severe osteopenia (∼ 60% lower bone mass) similar to mice globally expressing the knock-in mutation, consistent with the paradigm of innate immune-driven cryopyrinopathies. Because systemic inflammation may indirectly affect bone homeostasis, we engineered mice in which Nlrp3( D301N) is expressed specifically in osteoclasts, the cells that resorb bone. These mice also develop ∼ 50% lower bone mass due to increased osteolysis, but there is no systemic inflammation and no change in osteoclast number. Mechanistically, aside from its role in IL-1β maturation, Nlrp3( D301N) expression enhances osteoclast bone resorbing ability through reorganization of actin cytoskeleton while promoting the degradation of poly(ADP-ribose) polymerase 1, an inhibitor of osteoclastogenesis. Thus, NLRP3 inflammasome activation is not restricted to the production of proinflammatory mediators but also leads to cytokine-autonomous responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.