Journal ArticleDOI
Phenotypic instability of chondrocytes in osteoarthritis: on a path to hypertrophy
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TLDR
This review summarizes the data from the literature highlighting the loss of phenotypic stability and the hypertrophic differentiation of OA chondrocytes as central contributing factors to OA pathogenesis and outlines changes in DNA methylation status and alterations in NF‐κB signaling in OA.Abstract:
Articular chondrocytes are quiescent, fully differentiated cells responsible for the homeostasis of adult articular cartilage by maintaining cellular survival functions and the fine-tuned balance between anabolic and catabolic functions. This balance requires phenotypic stability that is lost in osteoarthritis (OA), a disease that affects and involves all joint tissues and especially impacts articular cartilage structural integrity. In OA, articular chondrocytes respond to the accumulation of injurious biochemical and biomechanical insults by shifting toward a degradative and hypertrophy-like state, involving abnormal matrix production and increased aggrecanase and collagenase activities. Hypertrophy is a necessary, transient developmental stage in growth plate chondrocytes that culminates in bone formation; in OA, however, chondrocyte hypertrophy is catastrophic and it is believed to initiate and perpetuate a cascade of events that ultimately result in permanent cartilage damage. Emphasizing changes in DNA methylation status and alterations in NF-κB signaling in OA, this review summarizes the data from the literature highlighting the loss of phenotypic stability and the hypertrophic differentiation of OA chondrocytes as central contributing factors to OA pathogenesis.read more
Citations
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Journal ArticleDOI
NF-κB Signaling Pathways in Osteoarthritic Cartilage Destruction.
TL;DR: The roles of NF-κB in OA chondrocytes and related signaling pathways are discussed to better understand pathological cartilage remodeling and provide potential therapeutic targets that can interfere with NF-σB signaling for OA treatment.
Journal ArticleDOI
Chondrocyte dedifferentiation and osteoarthritis (OA)
Edith Charlier,Céline Deroyer,Federica Ciregia,Olivier Malaise,Sophie Neuville,Zelda Plener,Michel Malaise,Dominique de Seny +7 more
TL;DR: Molecular knowledge underlying dedifferentiation process is presented, connections between dedifferentiated-like and OA are emphasized and therapeutic strategies aiming at the maintenance of chondrogenic phenotype are considered.
Journal ArticleDOI
Implantable and degradable antioxidant poly(ε-caprolactone)-lignin nanofiber membrane for effective osteoarthritis treatment.
Ruiming Liang,Jinmin Zhao,Bo Li,Peian Cai,Xian Jun Loh,Chuanhui Xu,Peng Chen,Dan Kai,Li Zheng +8 more
TL;DR: Electrospun PCL-lignin nanofibers show excellent antioxidant activity, low cytotoxicity and excellent anti-inflammatory effects as demonstrated using both H2O2-stimulated human chondrocytes and an OA rabbit model.
Journal ArticleDOI
The Role of Chondrocyte Morphology and Volume in Controlling Phenotype-Implications for Osteoarthritis, Cartilage Repair, and Cartilage Engineering.
TL;DR: An appreciation of the importance of chondrocyte volume and morphology for controlling the chondROcyte phenotype is advancing at a rapid pace and holds particular promise for developing strategies for protecting the chONDrocytes against deleterious changes and thereby maintaining healthy and resilient cartilage.
Journal ArticleDOI
Interplay between genetics and epigenetics in osteoarthritis.
TL;DR: It is found that many OA genetic risk signals interact with, map to or correlate with epigenetic mediators, which implies that epigenetic mechanisms, and their effect on gene expression, are a major conduit through which OA Genetic risk polymorphisms exert their functional effects.
References
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