Clock knockdown attenuated reactive oxygen species-mediated senescence of chondrocytes through restoring autophagic flux

Suppression of circadian clock protein cryptochrome 2 promotes osteoarthritis

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Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration

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Parkin clearance of dysfunctional mitochondria regulates ROS levels and increases survival of human chondrocytes

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The circadian clock regulates autophagy directly through the nuclear hormone receptor Nr1d1/Rev-erbα and indirectly via Cebpb/(C/ebpβ) in zebrafish

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Naturally occurring p16Ink4a-positive cells shorten healthy lifespan

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NPAS2 Compensates for Loss of CLOCK in Peripheral Circadian Oscillators

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Targeted deletion of Atg5 in chondrocytes promotes age-related osteoarthritis

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Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice

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Autophagy protects chondrocytes from glucocorticoids-induced apoptosis via ROS/Akt/FOXO3 signaling

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Cartilage-specific deletion of mTOR upregulates autophagy and protects mice from osteoarthritis

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The Circadian Clock in Murine Chondrocytes Regulates Genes Controlling Key Aspects of Cartilage Homeostasis

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Autophagy activation by rapamycin reduces severity of experimental osteoarthritis

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Autophagy modulates osteoarthritis-related gene expression in human chondrocytes

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Temporal orchestration of circadian autophagy rhythm by C/EBPβ

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Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with cell death and osteoarthritis

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