ArticleScience advances2022
Augmented ERAD (ER-associated degradation) activity in chondrocytes is necessary for cartilage development and maintenance.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Selenoprotein S Deficiency Induces Matrix Degradation Via TGF-β Pathway Leading to Cartilage Damage.Biological trace element research · 2026Article
- Limiting ER-associated degradation capacity triggers acute and chronic effects on insulin biosynthesis.The Journal of clinical investigation · 2026Article
- Clinical-grade iPSC-derived chondrogenic micropellets for treating advanced cartilage defects.Science advances · 2025Article
- Scaffold-free cell sheet therapies: clinical advances, global approval landscapes, and strategic directions to address regenerative medicine barriers.Stem cell research & therapy · 2025Review
- SEL1L regulates ER homeostasis in Sertoli cells but is dispensable for their function.Molecular biology of the cell · 2025Article
- Proteomic analysis of hydrogen peroxide-treated human chondrocytes shows endoplasmic reticulum stress, cytoskeleton remodeling, and altered secretome composition.Cell communication and signaling : CCS · 2025Article
- LIPUS Promotes Calcium Oscillation and Enhances Calcium Dependent Autophagy of Chondrocytes to Alleviate Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Blockade of the vaspin-AP-1 axis inhibits arthritis development.Experimental & molecular medicine · 2025Article
- Decoding Endoplasmic Reticulum Stress on Chondrocyte Driving Osteoarthritis Development through Integrating Single-Cell and Transcriptomic Profiling.International journal of medical sciences · 2025Article
- Integration of Network Pharmacology, Molecular Docking, and Experimental Validation to Identify the Effect of EGCG on Alleviating Chondrocyte Inflammatory Damage by Targeting ER Stress-STAT3 Crosstalk.Journal of inflammation research · 2025Article
- ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025Review
- Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications.Cell stress & chaperones · 2024Review
- Regulation of hepatic inclusions and fibrinogen biogenesis by SEL1L-HRD1 ERAD.Nature communications · 2024Article
- A multifunctional nanogel encapsulating layered double hydroxide for enhanced osteoarthritis treatment via protection of chondrocytes and ECM.Materials today. Bio · 2024Article
- Articular cartilage repair biomaterials: strategies and applications.Materials today. Bio · 2024Review
- Decreased expression of GEM in osteoarthritis cartilage regulates chondrogenic differentiation via Wnt/β-catenin signaling.Journal of orthopaedic surgery and research · 2023Article
- ER-associated degradation in cystinosis pathogenesis and the prospects of precision medicine.The Journal of clinical investigation · 2023Article
- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- Hepatic SEL1L-HRD1 ER-associated degradation regulates systemic iron homeostasis via ceruloplasmin.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Sirt3 Promotes Chondrogenesis, Chondrocyte Mitochondrial Respiration and the Development of High-Fat Diet-Induced Osteoarthritis in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrocytes secrete massive extracellular matrix (ECM) molecules that are produced, folded, and modified in the endoplasmic reticulum (ER). Thus, the ER-associated degradation (ERAD) complex-which removes misfolded and unfolded proteins to maintain proteostasis in the ER- plays an indispensable role in building and maintaining cartilage. Here, we examined the necessity of the ERAD complex in chondrocytes for cartilage formation and maintenance. We show that ERAD gene expression is exponentially increased during chondrogenesis, and disruption of ERAD function causes severe chondrodysplasia in developing embryos and loss of adult articular cartilage. ERAD complex malfunction also causes abnormal accumulation of cartilage ECM molecules and subsequent chondrodysplasia. ERAD gene expression is decreased in damaged cartilage from patients with osteoarthritis (OA), and disruption of ERAD function in articular cartilage leads to cartilage destruction in a mouse OA model.
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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.