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.
Dysfunctional mitochondria, the powerhouses of cells, are associated with development of intervertebral disc degeneration (IDD) and researchers are studying the mechanisms of mitochondrial quality control (MQC) to identify better treatments. IDD is a common and early-onset condition and one of the causes of low back pain. Current treatments address symptoms, not root causes, and a better understanding of IDD is needed. Cao Yang at Huazhong University of Science and Technology, Wuhan, China, and coworkers reviewed how cells maintain healthy mitochondria and the role of mitochondria in the development of IDD. The mechanisms of MQC include removing damaged mitochondria, generating new mitochondria, and managing harmful mitochondrial products. Treatments that target MQC show therapeutic promise, and further investigation of the roles played by the different mechanisms of MQC could lead to better treatments for this debilitating condition.