ArticleBioscience reports2017
Long-term load duration induces N-cadherin down-regulation and loss of cell phenotype of nucleus pulposus cells in a disc bioreactor culture.
Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- An overview of mechanical microenvironment and mechanotransduction in intervertebral disc degeneration.Experimental & molecular medicine · 2025Review
- Engineering Intervertebral Disc Regeneration: Biomaterials, Cell Sources and Animal Models.Cell proliferation · 2025Review
- The emerging role of Piezo1 in the musculoskeletal system and disease.Theranostics · 2024Review
- N-cadherin Alleviates Apoptosis and Senescence of Nucleus Pulposus Cells via Suppressing ROS-dependent ERS in the Hyper-osmolarity Microenvironment.International journal of medical sciences · 2024Article
- Integrins, cadherins and channels in cartilage mechanotransduction: perspectives for future regeneration strategies.Expert reviews in molecular medicine · 2021Review
- Mechanosensitive Ion Channel Piezo1 Activated by Matrix Stiffness Regulates Oxidative Stress-Induced Senescence and Apoptosis in Human Intervertebral Disc Degeneration.Oxidative medicine and cellular longevity · 2021Article
- Synbiotic supplementation with prebiotic green banana resistant starch and probiotic Bacillus coagulans spores ameliorates gut inflammation in mouse model of inflammatory bowel diseases.European journal of nutrition · 2020Article
- Transforming growth factor-β1-regulated Fas/FasL pathway activation suppresses nucleus pulposus cell apoptosis in an inflammatory environment.Bioscience reports · 2020Article
- High glucose promotes annulus fibrosus cell apoptosis through activating the JNK and p38 MAPK pathways.Bioscience reports · 2019Article
- Article
- Responses of apoptosis and matrix metabolism of annulus fibrosus cells to different magnitudes of mechanical tensionBioscience reports · 2019Article
- Static compression down-regulates N-cadherin expression and facilitates loss of cell phenotype of nucleus pulposus cells in a disc perfusion culture.Bioscience reports · 2018Article
Corrections and comments
- Retraction · 2024-08-22Concerns/Issues about Authorship/Affiliation · Duplication of/in Image · Compromised Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Objections by Author(s) ·
- Retracted
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term exposure to a mechanical load causes degenerative changes in the disc nucleus pulposus (NP) tissue. A previous study demonstrated that N-cadherin (N-CDH)-mediated signalling can preserve the NP cell phenotype. However, N-CDH expression and the resulting phenotype alteration in NP cells under mechanical compression remain unclear. The present study investigated the effects of the compressive duration on N-CDH expression and on the phenotype of NP cells in an
Indexed as
Identifiers
What OpenQuestion holds
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.