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Article

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 - 14 Feb 2023

Hecht Jacqueline T, Veerisetty Alka C, Hossain Mohammad G, Chiu Frankie, Posey Karen L

Abstract excerpt

Mutations in cartilage oligomeric matrix protein (COMP) causes protein misfolding and accumulation in chondrocytes that compromises skeletal growth and joint health in pseudoachondroplasia (PSACH), a severe dwarfing condition. Using the MT-COMP mice, a murine model of PSACH, we showed that pathological autophagy blockage was key to the intracellular accumulation of mutant-COMP. Autophagy is blocked by elevated...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 36835255
DOI: 10.3390/ijms24043845
PMCID: PMC9959842

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

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CurQ+, a Next-Generation Formulation of Curcumin, Ameliorates Growth Plate Chondrocyte Stress and Increases Limb Growth in a Mouse Model of Pseudoachondroplasia.PMID 36835255Read ↗

Early Resveratrol Treatment Mitigates Joint Degeneration and Dampens Pain in a Mouse Model of Pseudoachondroplasia (PSACH).Semantic proximity Read ↗

Novel therapeutic interventions for pseudoachondroplasia.Semantic proximity Read ↗

Antioxidant and anti-inflammatory agents mitigate pathology in a mouse model of pseudoachondroplasia.Semantic proximity Read ↗

Mutant cartilage oligomeric matrix protein (COMP) compromises bone integrity, joint function and the balance between adipogenesis and osteogenesis.Semantic proximity Read ↗

Health consequences of mutant cartilage oligomeric matrix protein and its relationship to abnormal growth and joint degeneration.Semantic proximity Read ↗

Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP.Semantic proximity Read ↗

A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.Semantic proximity Read ↗

An inducible cartilage oligomeric matrix protein mouse model recapitulates human pseudoachondroplasia phenotype.Semantic proximity Read ↗

Chop (Ddit3) Is Essential for D469del-COMP Retention and Cell Death in Chondrocytes in an Inducible Transgenic Mouse Model of PseudoachondroplasiaSemantic proximity Read ↗

The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review).Semantic proximity Read ↗

Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology.Semantic proximity Read ↗

Cartilage oligomeric matrix protein: COMPopathies and beyond.Semantic proximity Read ↗

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