ArticlePLoS biology2007
Surviving endoplasmic reticulum stress is coupled to altered chondrocyte differentiation and function.
Article in PLoS biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
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Who cites it
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.
- Integrative genomic analysis predicts novel functional enhancer-SNPs for bone mineral density.Human genetics · 2019Pooled it
- Integrated stress signaling pathways promote adaptive reprogramming for chondrocyte survival in Metaphyseal Chondrodysplasia Type Schmid.Bone research · 2026Article
- Mechanical Stimulation Drives Multicellular Synergy and Signaling Pathways in Developing Skeletal Tissues.Sports medicine (Auckland, N.Z.) · 2026Review
- A novel MMP13 frameshift variant causes short stature via enhanced MMP13-HSPA5 interaction and activated endoplasmic reticulum stress.Clinical and translational medicine · 2026Article
- COL10A1 beyond skeletal development: a hypertrophic chondrocyte-specific collagen emerging as a potential biomarker and tumor microenvironment regulator in solid cancers.American journal of cancer research · 2026Review
- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- ER Stress Is Associated with a "Mesenchymal Drift" in an Anaplastic Thyroid Carcinoma Cell Line.Cancers · 2025Article
- A Collagen10a1 mutation disrupts cell polarity in a medaka model for metaphyseal chondrodysplasia type Schmid.iScience · 2024Article
- A single-cell atlas of conventional central chondrosarcoma reveals the role of endoplasmic reticulum stress in malignant transformation.Communications biology · 2024Article
- Hypertrophic chondrocytes at the junction of musculoskeletal structures.Bone reports · 2023Article
- Hypomorphic and dominant-negative impact of truncated SOX9 dysregulates Hedgehog-Wnt signaling, causing campomelia.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Loss of DDRGK1 impairs IRE1α UFMylation in spondyloepiphyseal dysplasia.International journal of biological sciences · 2023Article
- A critical bioenergetic switch is regulated by IGF2 during murine cartilage development.Communications biology · 2022Article
- Collagen misfolding mutations: the contribution of the unfolded protein response to the molecular pathology.Connective tissue research · 2022Review
- 4PBA reduces growth deficiency in osteogenesis imperfecta by enhancing transition of hypertrophic chondrocytes to osteoblasts.JCI insight · 2022Article
- Estradiol Inhibits ER Stress-Induced Apoptosis in Chondrocytes and Contributes to a Reduced Osteoarthritic Cartilage Degeneration in Female Mice.Frontiers in cell and developmental biology · 2022Article
- ER Stress in ERp57 Knockout Knee Joint Chondrocytes Induces Osteoarthritic Cartilage Degradation and Osteophyte Formation.International journal of molecular sciences · 2021Article
- Dynamic regulation of mitochondrial-endoplasmic reticulum crosstalk during stem cell homeostasis and aging.Cell death & disease · 2021Review
- Role of autophagy in intervertebral disc and cartilage function: implications in health and disease.Matrix biology : journal of the International Society for Matrix Biology · 2021Review
- Effects of an Environmentally Relevant Mixture of Organophosphate Esters Derived From House Dust on Endochondral Ossification in Murine Limb Bud Cultures.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 4 countries.
Funding
Abstract
In protein folding and secretion disorders, activation of endoplasmic reticulum (ER) stress signaling (ERSS) protects cells, alleviating stress that would otherwise trigger apoptosis. Whether the stress-surviving cells resume normal function is not known. We studied the in vivo impact of ER stress in terminally differentiating hypertrophic chondrocytes (HCs) during endochondral bone formation. In transgenic mice expressing mutant collagen X as a consequence of a 13-base pair deletion in Col10a1 (13del), misfolded alpha1(X) chains accumulate in HCs and elicit ERSS. Histological and gene expression analyses showed that these chondrocytes survived ER stress, but terminal differentiation is interrupted, and endochondral bone formation is delayed, producing a chondrodysplasia phenotype. This altered differentiation involves cell-cycle re-entry, the re-expression of genes characteristic of a prehypertrophic-like state, and is cell-autonomous. Concomitantly, expression of Col10a1 and 13del mRNAs are reduced, and ER stress is alleviated. ERSS, abnormal chondrocyte differentiation, and altered growth plate architecture also occur in mice expressing mutant collagen II and aggrecan. Alteration of the differentiation program in chondrocytes expressing unfolded or misfolded proteins may be part of an adaptive response that facilitates survival and recovery from the ensuing ER stress. However, the altered differentiation disrupts the highly coordinated events of endochondral ossification culminating in chondrodysplasia.
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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.