ArticleHuman molecular genetics2015
Antioxidant and anti-inflammatory agents mitigate pathology in a mouse model of pseudoachondroplasia.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 40 citations in OpenAlex.
- Genotype-phenotype correlations in PSACH/EDM1 patients withFrontiers in endocrinology · 2026Review
- ElevatedInternational journal of molecular sciences · 2025Article
- Loss of CHOP Prevents Joint Degeneration and Pain in a Mouse Model of Pseudoachondroplasia.International journal of molecular sciences · 2024Article
- Thrombospondins: Conserved mediators and modulators of metazoan extracellular matrix.International journal of experimental pathology · 2024Review
- Curcumin and Resveratrol: Nutraceuticals with so Much Potential for Pseudoachondroplasia and Other ER-Stress Conditions.Biomolecules · 2024Review
- Early Resveratrol Treatment Mitigates Joint Degeneration and Dampens Pain in a Mouse Model of Pseudoachondroplasia (PSACH).Biomolecules · 2023Article
- CurQ+, a Next-Generation Formulation of Curcumin, Ameliorates Growth Plate Chondrocyte Stress and Increases Limb Growth in a Mouse Model of Pseudoachondroplasia.International journal of molecular sciences · 2023Article
- What to Expect of Feeding Abilities and Nutritional Aspects in Achondroplasia Patients: A Narrative Review.Genes · 2023Review
- Clinical, Biochemical, Radiological, Genetic and Therapeutic Analysis of Patients with COMP Gene Variants.Calcified tissue international · 2022Article
- The role of Wnt/mTOR signaling in spinal cord injury.Journal of clinical orthopaedics and trauma · 2022Review
- Structure, evolution and expression of zebrafish cartilage oligomeric matrix protein (COMP, TSP5). CRISPR-Cas mutants show a dominant phenotype in myosepta.Frontiers in endocrinology · 2022Article
- Primary Osteoarthritis Early Joint Degeneration Induced by Endoplasmic Reticulum Stress Is Mitigated by Resveratrol.The American journal of pathology · 2021Article
- Joint Degeneration in a Mouse Model of Pseudoachondroplasia: ER Stress, Inflammation, and Block of Autophagy.International journal of molecular sciences · 2021Article
- COMP: A Potential Early Biomarker of RAS After Lung Transplantation.Transplantation direct · 2021Article
- Article
- Mutant COMP shapes growth and development of skull and facial structures in mice and humans.Molecular genetics & genomic medicine · 2020Article
- New developments in chondrocyte ER stress and related diseases.F1000Research · 2020Review
- Obesity in achondroplasia patients: from evidence to medical monitoring.Orphanet journal of rare diseases · 2019Review
- A novel mutation in exon 11 of COMP gene in a Chinese family with pseudoachondroplasia.Genes & diseases · 2019Article
- Novel mTORC1 Mechanism Suggests Therapeutic Targets for COMPopathies.The American journal of pathology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Pseudoachondroplasia (PSACH), a severe short-limb dwarfing condition, results from mutations that cause misfolding of the cartilage oligomeric matrix protein (COMP). Accumulated COMP in growth plate chondrocytes activates endoplasmic reticulum stress, leading to inflammation and chondrocyte death. Using a MT-COMP mouse model of PSACH that recapitulates the molecular and clinical PSACH phenotype, we previously reported that oxidative stress and inflammation play important and unappreciated roles in PSACH pathology. In this study, we assessed the ability of antioxidant and anti-inflammatory agents to affect skeletal and cellular pathology in our mouse model of PSACH. Treatment of MT-COMP mice with aspirin or resveratrol from birth to P28 decreased mutant COMP intracellular retention and chondrocyte cell death, and restored chondrocyte proliferation. Inflammatory markers associated with cartilage degradation and eosinophils were present in the joints of untreated juvenile MT-COMP mice, but were undetectable in treated mice. Most importantly, these treatments resulted in significantly increased femur length. This is the first and only therapeutic approach shown to mitigate both the chondrocyte and long-bone pathology of PSACH in a mouse model and suggests that reducing inflammation and oxidative stress early in the disease process may be a novel approach to treat this disorder.
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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.