ArticleiScience2021
TRPV6 is a potential regulator of bone resorption in bone loss induced by estrogen deficiency.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Disruption of Claudin-2 and Trpv6 Results in Hypocalcemia, Hypercalciuria, and Altered Bone Microarchitecture in Mice.Acta physiologica (Oxford, England) · 2026Article
- The role of calcium ions and the transient receptor potential vanilloid (TRPV) channel in bone remodelling and orthodontic tooth movement.Molecular biology reports · 2025Review
- Bone equilibria and disruptions.Journal of the Pediatric Orthopaedic Society of North America · 2024Article
- Integration of single-cell and RNA-seq data to explore the role of focal adhesion-related genes in osteoporosis.Journal of cellular and molecular medicine · 2024Article
- Sex-specific alteration in human muscle transcriptome with age.GeroScience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The precise effect of estrogen (E2) on osteoclast function is still poorly understood. The aim of this study was to investigate the potential role of transient receptor potential vanilloid 6 (TRPV6) in E2-mediated osteoclast function and to characterize the relevant underlying mechanisms. Here, we found that Trpv6 is drastically decreased in ovariectomy operation animals and the administration of E2 results in an increased expression of Trpv6 in osteoclasts. In contrast, Trpv6 depletion significantly blocked the inhibitory effects of E2 on bone resorption activity, and silencing Trpv6 alleviated E2-induced osteoclast apoptosis. In addition, we found that E2 regulates the transcription of Trpv6 through ERα, by interacting with C/EBPβ and NF-κB. Chip assay analysis indicated that C/EBPβ regulates Trpv6 transcription by binding to Trpv6 promoter fragments -1,866 nt to -1,761 nt and -2,685 nt to -2,580 nt, whereas NF-κB binds to the -953 nt to -851 nt region. We conclude that TRPV6 has a significant effect on E2-mediated osteoclast function.
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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.