Intervertebral disc degeneration (IVDD) is an aging disease that results in a low quality of life and heavy socioeconomic burden. The mitochondrial unfolded protein response (UPR) take part in various aging-related diseases. Our research intents to explore the role and underlying mechanism of UPR in IVDD. Nucleus pulposus (NP) cells were exposed to IL-1β and nicotinamide riboside (NR) served as UPR inducer to treat NP cells. Detection of ATP, NAD + and NADH were used to determine the function of mitochondria. MRI, Safranin O-fast green and Immunohistochemical examination were used to determine the degree of IVDD in vivo. In this study, we discovered that UPR was increased markedly in the NP cells of human IVDD tissues than in healthy controls. In vitro, UPR and mitophagy levels were promoted in NP cells treated with IL-1β. Upregulation of UPR by NR and Atf5 overexpression inhibited NP cell apoptosis and further improved mitophagy. Silencing of Pink1 reversed the protective effects of NR and inhibited mitophagy induced by the UPR. In vivo, NR might attenuate the degree of IDD by activating the UPR in rats. In summary, the UPR was involved in IVDD by regulating Pink1-induced mitophagy. Mitophagy induced by the UPR might be a latent treated target for IVDD.
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| http://dx.doi.org/10.1007/s10565-024-09854-9 | DOI Listing |
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