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Article

The ClockΔ19 mutation promotes osteoarthritis via impairing SIRT3-mediated mitochondrial homeostasis in mice.

Journal of orthopaedic surgery and research - 30 Jun 2026

Zhang Qijing, Liu Yanhong, Chen Yuwen, Zhou Yanqing, Yan Zuoqin, Qian Ruizhe, Lu Chao, Hua Bingxuan

Abstract excerpt

BACKGROUND: Osteoarthritis (OA) is a chronic degenerative joint disease characterized by cartilage breakdown and disrupted joint homeostasis. Mitochondrial dysfunction in chondrocytes contributes to cartilage degeneration, but the mechanisms linking circadian dysregulation to mitochondrial homeostasis in OA remain incompletely understood. ClockΔ19 mice are a well-established model of impaired CLOCK-dependent...

Read the complete abstract on PubMed

Topics

Animals
Sirtuin 3
Homeostasis
Mice
Osteoarthritis
Mitochondria
CLOCK Proteins

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Humans

Chondrocytes

Mutation

Male

Cells, Cultured

Circadian Rhythm

Disease Models, Animal

Source

Open in PubMed Open full text

Identifiers

PMID: 42374427
DOI: 10.1186/s13018-026-07050-5
PMCID: PMC13584504

Genes

SIRT3
CLOCK
SOD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 25 Oct 2026.

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