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Keywords: intervertebral disc degeneration; autophagy; low back pain; autophagy-targeting compounds; ECM degradation EN intervertebral disc degeneration autophagy low back pain autophagy-targeting compounds ECM degradation N.PAG N.PAG 30 08/29/22 20220801 NES 220801 1. This review of recent studies on autophagy-regulated IVD degeneration lays a foundation for further research aimed at elucidating the underlying mechanisms of IVDD and understanding the contribution of autophagy, the ultimate goal of which is to develop novel approaches to IVDD treatment and prevention. The lncRNA-FAM83H-AS1 pathway preserves IVD tissue homeostasis and reduces inflammation-related discomfort by inhibiting miR-22-3p, which promotes NP cell proliferation [[292]]. lncRNA-H19 increases autophagy and death in NP cells, exacerbating IVDD via the miR-139/CXCR4/NF-B axis [[293]]. Autophagy-Targeting Compounds in IVDD Although autophagy may have a dual role in IVDD, most recent investigations show that it protects against IVDD. [Extracted from the article]

The development of osteoarthritis (OA), the most common form of arthritis, is commonly associated with oxidative stress. Indeed, the lack of antioxidant responses largely increases OA incidence. OA is a leading cause of disability in the elderly, which reduces the quality of life and places high socioeconomic burdens on them. Several polyphenolic compounds, including chlorogenic acid (CGA), have shown cytoprotective effects via their antioxidant activity, but the exact mechanism (s) remain elusive. In this study, we demonstrated how CGA protects human chondrocytes against H 2 O 2 -induced apoptosis. The cytoprotective effect by CGA in 500 μM hydrogen peroxide-treated C28/I2 cells was evaluated by cell viability, TUNEL assay, and Western blotting analyses, and autophagy assessment was further performed by AO and MDC staining and tandem mRFP-GFP fluorescence analyses. Treatment of CGA to the human chondrocytes under oxidative stress significantly decreased apoptosis markers, such as cleaved caspase 3 and cleaved PARP, and increased anti-apoptotic marker Bcl-xL and the antioxidant response proteins NRF2 and NF-κB. Furthermore, CGA-dependent activation of antioxidant response proteins NRF2 and NF-κB and its protective effects in chondrocytes depended on autophagy. Indeed, CGA treatment and autophagy induction significantly decreased reactive oxygen species (ROS)–induced apoptosis. CGA exhibited the protective effect to human chondrocyte C28/I2 cells against oxidative stress-induced cell death by activating autophagy. These findings indicate that CGA is a potential therapeutic agent for the development of OA drugs. [ABSTRACT FROM AUTHOR]