Abstract
Autophagy is involved in different degenerative diseases and it may control epigenetic modifications, metabolic processes, stem cells differentiation as well as apoptosis. Autophagy plays a key role in maintaining the homeostasis of cartilage, the tissue produced by chondrocytes; its impairment has been associated to cartilage dysfunctions such as osteoarthritis (OA). Due to their location in a reduced oxygen context, both differentiating and mature chondrocytes are at risk of premature apoptosis, which can be prevented by autophagy. AutophagomiRNAs, which regulate the autophagic process, have been found differentially expressed in OA. AutophagomiRNAs, as well as other regulatory molecules, may also be useful as therapeutic targets. In this review, we describe and discuss the role of autophagy in OA, focusing mainly on the control of autophagomiRNAs in OA pathogenesis and their potential therapeutic applications.
Highlights
Chondrogenesis, the process by which cartilage is formed, occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation
Chondrogenesis is subject to complex regulation by several interplaying factors such as fibroblast growth factor (FGF), transforming growth factor β (TGFβ), bone morphogenetic proteins (BMPs) and Wnt signaling pathways
Instead, chondrocytes are responsible for the production and homeostatic maintenance of the extracellular matrix (ECM) components
Summary
Chondrogenesis, the process by which cartilage is formed, occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation. Instead, chondrocytes are responsible for the production and homeostatic maintenance of the extracellular matrix (ECM) components. Besides playing a crucial role in adaptive response to different stimuli, it is required for intracellular quality control and is involved in removing and recycling misfolded proteins, damaged organelles or dysfunctional cell components [4]. 2021i,n22g, 2a70c0rucial role in adaptive response to different stimuli, it is required for intracellular quality control and is involved in removing and recycling misfolded proteins, damaged organelles or dysfunctional cell components [4]. OA, a chronic, age-related degenerative disease of articular cartilage, is associated with dramatic changes in cartilage homeostasis, due to an imbalance between degradation and synthesis by chondrocytes. Disease progression is usually slow but can lead to joint failure with pain and disability, with considerable socio-economic impact [8]
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