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Hydrostatic Compress Force Enhances the Viability and Decreases the Apoptosis of Condylar Chondrocytes through Integrin-FAK-ERK/PI3K Pathway

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Laboratory of Rheumatology, Groupe Interdisciplinaire de Génoprotéomique Appliquée (GIGA) Research, Centre Hospitalier Universitaire (CHU) de Liège, University of Liège, 4000 Liège, Belgium
Author to whom correspondence should be addressed.
Academic Editors: Charles J. Malemud and Ali Mobasheri
Int. J. Mol. Sci. 2016, 17(12), 2146;
Received: 29 October 2016 / Revised: 5 December 2016 / Accepted: 12 December 2016 / Published: 20 December 2016
(This article belongs to the Special Issue Apoptotic Chondrocytes and Osteoarthritis)
Osteoarthritis (OA) is a joint pathology characterized by progressive cartilage degradation. Medical care is mainly based on alleviating pain symptoms. Compelling studies report the presence of empty lacunae and hypocellularity in cartilage with aging and OA progression, suggesting that chondrocyte cell death occurs and participates to OA development. However, the relative contribution of apoptosis per se in OA pathogenesis appears complex to evaluate. Indeed, depending on technical approaches, OA stages, cartilage layers, animal models, as well as in vivo or in vitro experiments, the percentage of apoptosis and cell death types can vary. Apoptosis, chondroptosis, necrosis, and autophagic cell death are described in this review. The question of cell death causality in OA progression is also addressed, as well as the molecular pathways leading to cell death in response to the following inducers: Fas, Interleukin-1β (IL-1β), Tumor Necrosis factor-α (TNF-α), leptin, nitric oxide (NO) donors, and mechanical stresses. Furthermore, the protective role of autophagy in chondrocytes is highlighted, as well as its decline during OA progression, enhancing chondrocyte cell death; the transition being mainly controlled by HIF-1α/HIF-2α imbalance. Finally, we have considered whether interfering in chondrocyte apoptosis or promoting autophagy could constitute therapeutic strategies to impede OA progression. View Full-Text
Keywords: osteoarthritis; apoptosis; necrosis; chondroptosis; autophagy; chondrocytes osteoarthritis; apoptosis; necrosis; chondroptosis; autophagy; chondrocytes
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MDPI and ACS Style

Charlier, E.; Relic, B.; Deroyer, C.; Malaise, O.; Neuville, S.; Collée, J.; Malaise, M.G.; De Seny, D. Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis. Int. J. Mol. Sci. 2016, 17, 2146.

AMA Style

Charlier E, Relic B, Deroyer C, Malaise O, Neuville S, Collée J, Malaise MG, De Seny D. Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis. International Journal of Molecular Sciences. 2016; 17(12):2146.

Chicago/Turabian Style

Charlier, Edith, Biserka Relic, Céline Deroyer, Olivier Malaise, Sophie Neuville, Julie Collée, Michel G. Malaise, and Dominique De Seny. 2016. "Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis" International Journal of Molecular Sciences 17, no. 12: 2146.

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