Current Drug Targets

Francis J. Castellino
Kleiderer-Pezold Professor of Biochemistry
Director, W.M. Keck Center for Transgene Research
Dean Emeritus, College of Science
230 Raclin-Carmichael Hall, University of Notre Dame
Notre Dame, IN 46556
USA

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Mitochondrial Pathology in Osteoarthritic Chondrocytes

Author(s): Longhuo Wu, Haiqing Liu, Linfu Li, Hai Liu, Qilai Cheng, Hongliang Li and Hao Huang

Affiliation: College of Pharmacy, Gannan Medical University, Ganzhou 341000, China.

Keywords: Aging, chondrocytes, leptin, mitochondrial pathology, obesity, osteoarthritis, pro-inflammatory cytokines, ROS.

Abstract:

Osteoarthritis (OA) is a chronic degenerative disease leading to aberrance of cartilage structures with unclear or multifactorial mechanisms. Recently, a great portion of research endeavor to explore the molecular mechanisms of OA in focusing on the mitochondrial pathology. Mitochondrial respiratory chain (MRC) produces reactive oxygen species (ROS), which in turn impair mtDNA integrity and link to cartilage degradation in OA. The fine-tuning between ROS and antioxidant within chondrocytes ensures cartilage homeostasis. With disturbance from pro-inflammatory cytokines, oxidative stress synergistically instigates cellular signaling and exacerbates mitochondrial pathology, which may affect several pathways implicated in OA cartilage degradation, including oxidative stress, increase of cytokine-induced chondrocytes inflammation and matrix catabolism, aging and senescence, obesity-related pathology, and cartilage matrix calcification. Unveiling the molecular mechanisms of mitochondrial function in OA pathogenesis and progression is essential for providing relevant therapeutic targets. These suggest that efficient protection and improvement of mitochondrial activity can be a therapeutic alternative for OA patients.

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Article Details

VOLUME: 15
ISSUE: 7
Page: [710 - 719]
Pages: 10
DOI: 10.2174/1389450115666140417120305