ArticleCell proliferation2021
The calcium channel TRPV6 is a novel regulator of RANKL-induced osteoclastic differentiation and bone absorption activity through the IGF-PI3K-AKT pathway.
Article in Cell proliferation, 2021. 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, 31 citations in OpenAlex.
- Pathological calcium overload impairs skeletal muscle regeneration through sustained NFAT-dependent proliferative signaling.Experimental & molecular medicine · 2026Article
- Transcriptomic insights into exercise-induced trabecular bone microarchitectural adaptations following combined aerobic and resistance training in mice.Scientific reports · 2026Article
- Cadmium Uptake into Rat Osteoblast UMR-106 Cells is Mediated via Multiple Pathways.Biological trace element research · 2026Article
- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 2025Review
- The role of calcium ions and the transient receptor potential vanilloid (TRPV) channel in bone remodelling and orthodontic tooth movement.Molecular biology reports · 2025Review
- Targeting TRPC channels for control of arthritis-induced bone erosion.Science advances · 2025Article
- Isonardosinone suppresses osteoclastogenesis through TRAF2/TRAF6-mediated disruption of calcium signaling and coordinate inhibition of MAPK/NF-κB pathways.BBA advances · 2025Article
- The role of transient receptor potential channels in chronic kidney disease-mineral and bone disorder.Frontiers in pharmacology · 2025Review
- Neoandrographolide inhibits mature osteoclast differentiation to alleviate bone loss and treat osteoporosis.Frontiers in pharmacology · 2025Article
- Transient Receptor Potential Vanilloid 6 Modulates Aberrant Axonal Sprouting in a Mouse Model of Pilocarpine-Induced Epilepsy.Molecular neurobiology · 2024Article
- The role of calcium channels in osteoporosis and their therapeutic potential.Frontiers in endocrinology · 2024Review
- The Mechanism of Action and Experimental Verification of Narenmandula in the Treatment of Postmenopausal Osteoporosis.Combinatorial chemistry & high throughput screening · 2024Article
- Characterization of the TRPV6 calcium channel-specific phenotype by RNA-seq in castration-resistant human prostate cancer cells.Frontiers in genetics · 2023Article
- Niobium promotes fracture healing in rats by regulating the PI3K-Akt signalling pathway: AnJournal of orthopaedic translation · 2022Article
- Roles of calcium signaling in cancer metastasis to bone.Exploration of targeted anti-tumor therapy · 2022Review
- TRPV6 is a potential regulator of bone resorption in bone loss induced by estrogen deficiency.iScience · 2021Article
- MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process.Annals of translational medicine · 2021Article
- The calcium channel TRPV6 is a novel regulator of RANKL-induced osteoclastic differentiation and bone absorption activity through the IGF-PI3K-AKT pathway.Cell proliferation · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
objectivesCalcium ion signals are important for osteoclast differentiation. Transient receptor potential vanilloid 6 (TRPV6) is a regulator of bone homeostasis. However, it was unclear whether TRPV6 was involved in osteoclast formation. Therefore, the aim of this study was to evaluate the role of TPRV6 in bone metabolism and to clarify its regulatory role in osteoclasts at the cellular level. MATERIALS AND
methodsBone structure and histological changes in Trpv6 knockout mice were examined using micro-computed tomography and histological analyses. To investigate the effects of Trpv6 on osteoclast function, we silenced or overexpressed Trpv6 in osteoclasts via lentivirus transfection, respectively. Osteoclast differentiation and bone resorption viability were measured by tartrate-resistant acid phosphatase (TRAP) staining and pit formation assays. The expression of osteoclast marker genes, including cathepsin k, DC-STAMP, Atp6v0d2 and TRAP, was measured by qRT-PCR. Cell immunofluorescence and Western blotting were applied to explore the mechanisms by which the IGF-PI3K-AKT pathway was involved in the regulation of osteoclast formation and bone resorption by Trpv6.
resultsWe found that knockout of Trpv6 induced osteoporosis and enhanced bone resorption in mice, but did not affect bone formation. Further studies showed that Trpv6, which was distributed on the cell membrane of osteoclasts, acted as a negative regulator for osteoclast differentiation and function. Mechanistically, Trpv6 suppressed osteoclastogenesis by decreasing the ratios of phosphoprotein/total protein in the IGF-PI3K-AKT signalling pathway. Blocking of the IGF-PI3K-AKT pathway significantly alleviated the inhibitory effect of Trpv6 on osteoclasts formation.
conclusionsOur study confirmed the important role of Trpv6 in bone metabolism and clarified its regulatory role in osteoclasts at the cellular level. Taken together, this study may inspire a new strategy for the treatment of osteoporosis.
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