ArticleJournal of cellular and molecular medicine2024
Excessive load promotes temporomandibular joint chondrocyte apoptosis via Piezo1/endoplasmic reticulum stress pathway.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed.
- Review
- Submolecular modulation of PIEZO1 mechanotransduction with wireless tailor-made nanoswitches.Bioactive materials · 2026Article
- Review
- PIEZO1 variants that reduce open channel probability are associated with familial osteoarthritis.The Journal of biological chemistry · 2026Article
- Exploring the Therapeutic Potential of Piezo1 in Ageing-Related Neurodegenerative Diseases.Journal of molecular neuroscience : MN · 2026Review
- Next-Generation Joint-on-a-Chip: Toward Precision Mechanical Control in Multi-Tissue Systems.Nano-micro letters · 2026Review
- A validated SSAM-FEA framework for the rat knee reproduces varus-induced contact redistribution in a meniscus-deficient setting.Frontiers in bioengineering and biotechnology · 2026Article
- Biomechanical research using advanced micro-nano devices: In-Vitro cell Characterization focus.Journal of advanced research · 2025Review
- Piezo1 in heart failure: A new perspective from cytomechanical sensing to diverse cellular pathways.Molecular biology reports · 2025Review
- A Cross-Tissue Transcriptome-Wide Association Study Identified Susceptibility Genes for Intervertebral Disc Degeneration.JOR spine · 2025Article
- Tensile stress promotes the chondrogenic ability of condylar cartilage stem/progenitor cells in the temporomandibular joint via the Piezo1-CaStem cell research & therapy · 2025Article
- Mechanosensitive channel Piezo1 in calcium dynamics: structure, function, and emerging therapeutic strategies.Frontiers in molecular biosciences · 2025Review
- Article
- Excessive load promotes temporomandibular joint chondrocyte apoptosis via Piezo1/endoplasmic reticulum stress pathway.Journal of cellular and molecular medicine · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Excessive load on the temporomandibular joint (TMJ) is a significant factor in the development of TMJ osteoarthritis, contributing to cartilage degeneration. The specific mechanism through which excessive load induces TMJ osteoarthritis is not fully understood; however, mechanically-activated (MA) ion channels play a crucial role. Among these channels, Piezo1 has been identified as a mediator of chondrocyte catabolic responses and is markedly increased in osteoarthritis. Our observations indicate that, under excessive load conditions, endoplasmic reticulum stress in chondrocytes results in apoptosis of the TMJ chondrocytes. Importantly, using the Piezo1 inhibitor GsMTx4 demonstrates its potential to alleviate this condition. Furthermore, Piezo1 mediates endoplasmic reticulum stress in chondrocytes by inducing calcium ion influx. Our research substantiates the role of Piezo1 as a pivotal ion channel in mediating chondrocyte overload. It elucidates the link between excessive load, cell apoptosis, and calcium ion influx through Piezo1. The findings underscore Piezo1 as a key player in the pathogenesis of TMJ osteoarthritis, shedding light on potential therapeutic interventions for this condition.
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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 Socratic graph.