Autophagy in osteoarthritis

Li, Yusheng; Zhang, Fang‐Jie; Zeng, Chao; Luo, Wei; Xiao, Wenfeng; Gao, Shu‐guang; Lei, Guanghua

doi:10.1016/j.jbspin.2015.06.009

Cited by 127 publications

(109 citation statements)

References 72 publications

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“…Reports showed that dysfunctional cellular organelles and macromolecules increased remarkably in the degeneration cartilage, interrupting cell function. Meanwhile, autoghagy can degrade these molecules, inhibiting chondrocyte apoptosis and blocking the degeneration of articular cartilages and OA development [52][53][54]. Additionally, evidence showed that ROS also interacted with autophagy during the degenerative process of cartilages [55,56].…”

Section: Ampk/mtor Signaling Pathway Is Involved In Gapn-induced Automentioning

confidence: 99%

Globular Adiponectin Attenuated H2O2-Induced Apoptosis in Rat Chondrocytes by Inducing Autophagy Through the AMPK/ mTOR Pathway

Cui

Ding

et al. 2017

Cell Physiol Biochem

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Background/Aims: Chondrocyte apoptosis is closely related to the development and progression of osteoarthritis. Global adiponectin (gAPN), secreted from adipose tissue, possesses potent anti-inflammatory and antiapoptotic properties in various cell types. This study aimed to investigate the role of autophagy induced by gAPN in the suppression of H 2 O 2 -induced apoptosis and the potential mechanism of gAPN-induced autophagy in chondrocytes. Methods: H 2 O 2 was used to induce apoptotic injury in rat chondrocytes. CCK-8 assay was performed to determine the viability of cells treated with different concentrations of gAPN with or without H 2 O 2 . Cell apoptosis was detected by flow cytometry and TUNEL staining. Mitochondrial membrane potential was examined using JC-1 fluorescence staining assay. The autophagy inhibitors 3-MA and Bafilomycin A1 were used to treat cells and then evaluate the effect of gAPN-induced autophagy. To determine the downstream pathway, chondrocytes were preincubated with the AMPK inhibitor Compound C. Beclin-1, LC3B, P62 and apoptosisrelated proteins were identified by Western blot analysis. Results: H 2 O 2 (400 μM)-induced chondrocytes apoptosis and caspase-3 activation were attenuated by gAPN (0.5 μg/mL). gAPN increased Bcl-2 expression and decreased Bax expression. The loss of mitochondrial membrane potential induced by H 2 O 2 was also abolished by gAPN. Furthermore, the antiapoptotic effect of gAPN was related to gAPN-induced autophagy by increased formation of Beclin-1 and LC3B and P62 degradation. In particular, the inhibition of gAPN-induced autophagy by 3-MA prevented the protective effect of gAPN on apoptosis induced by H 2 O 2 . Moreover, gAPN increased p-AMPK expression and decreased p-mTOR expression. Compound C partly suppressed the expression of autophagy-related proteins and restored the expression of p-mTOR suppressed by gAPN. Thus, the AMPK/mTOR pathway played an important role

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Section: Ampk/mtor Signaling Pathway Is Involved In Gapn-induced Automentioning

confidence: 99%

Globular Adiponectin Attenuated H2O2-Induced Apoptosis in Rat Chondrocytes by Inducing Autophagy Through the AMPK/ mTOR Pathway

Cui

Ding

et al. 2017

Cell Physiol Biochem

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“…Alzheimer's and Parkinson's) 79 and vascular 80 diseases, cancer, 81 diabetes, 82 obesity, 83 rheumatoid arthritis, 84 and osteoarthritis. 85 Studies suggest that dysregulation of autophagy may also be associated with the process of bone loss and subsequent osteoporosis. 27,86 Recently, pharmacological inhibition with chloroquine and genetic inhibition by the selective deletion of the Atg7 gene in monocytes have been shown to reduce osteoclastogenesis and decrease bone loss in animal models.…”

Section: Autophagy Bone Loss and Osteoporosismentioning

confidence: 99%

Osteoporosis and autophagy: What is the relationship?

Florencio‐Silva

Sasso

Simões

et al. 2017

Rev. Assoc. Med. Bras.

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Autophagy is a survival pathway wherein non-functional proteins and organelles are degraded in lysosomes for recycling and energy production. Therefore, autophagy is fundamental for the maintenance of cell viability, acting as a quality control process that prevents the accumulation of unnecessary structures and oxidative stress. Increasing evidence has shown that autophagy dysfunction is related to several pathologies including neurodegenerative diseases and cancer. Moreover, recent studies have shown that autophagy plays an important role for the maintenance of bone homeostasis. For instance, in vitro and animal and human studies indicate that autophagy dysfunction in bone cells is associated with the onset of bone diseases such as osteoporosis. This review had the purpose of discussing the issue to confirm whether a relationship between autophagy dysfunction and osteoporosis exits.

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“…In recent years, autophagy has become a research hot. There is a large and growing body of evidence that autophagy disfunction is extensively involved in the development of many degenerative diseases, including osteoarthritis [19,20], neurodegeneration [17,21] and IDD [22]. In this review, we will focus mainly on the recent findings regarding the autophagic process and the involvement of autophagy in disc degeneration.…”

Section: Accepted Manuscriptmentioning

confidence: 99%