Mitochondrial quality control in intervertebral disc degeneration

Yu Song; Saideng Lu; Wen Geng; Xiaobo Feng; Rongjin Luo; Gaocai Li; Cao Yang

doi:10.1038/s12276-021-00650-7

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자료유형: 학술저널

저자정보: Yu Song (Huazhong University of Science and Technology) Saideng Lu (Huazhong University of Science and Technology) Wen Geng (Huazhong University of Science and Technology) Xiaobo Feng (Huazhong University of Science and Technology) Rongjin Luo (Huazhong University of Science and Technology) Gaocai Li (Huazhong University of Science and Technology) Cao Yang (Huazhong University of Science and Technology)

저널정보: 대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제53권

발행연도: 2021.7

수록면: 1 - 10 (10page)

DOI: 10.1038/s12276-021-00650-7

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Intervertebral disc degeneration (IDD) is a common and early-onset pathogenesis in the human lifespan that can increase the risk of low back pain. More clarification of the molecular mechanisms associated with the onset and progression of IDD is likely to help establish novel preventive and therapeutic strategies. Recently, mitochondria have been increasingly recognized as participants in regulating glycolytic metabolism, which has historically been regarded as the main metabolic pathway in intervertebral discs due to their avascular properties. Indeed, mitochondrial structural and functional disruption has been observed in degenerated nucleus pulposus (NP) cells and intervertebral discs. Multilevel and well-orchestrated strategies, namely, mitochondrial quality control (MQC), are involved in the maintenance of mitochondrial integrity, mitochondrial proteostasis, the mitochondrial antioxidant system, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis. Here, we address the key evidence and current knowledge of the role of mitochondrial function in the IDD process and consider how MQC strategies contribute to the protective and detrimental properties of mitochondria in NP cell function. The relevant potential therapeutic treatments targeting MQC for IDD intervention are also summarized. Further clarification of the functional and synergistic mechanisms among MQC mechanisms may provide useful clues for use in developing novel IDD treatments.

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