Low back pain (LBP) is a common clinical problem and a major cause of physical disability, imposing a prominent socioeconomic burden. Intervertebral disc degeneration (IDD) has been considered the main cause of LBP. The current treatments have limited efficacy because they cannot address the underlying degeneration. With an increased understanding of the complex pathological mechanism of IDD, various medications and biological reagents have been used for intradiscal injection for the treatment of LBP. There is increasing clinical evidence showing the benefits of these therapies on symptomatic relief and their potential for disc repair and regeneration by targeting the disrupted pathways underlying the cause of the disease. A brief overview of the potential and limitations for these therapies are provided in this review, based on the recent and available data from clinical trials and systematic reviews.Finally, future perspectives are discussed.intervertebral disc degeneration, intradiscal injection, low back pain | INTRODUCTIONLow back pain (LBP) is a common symptom that occurs below the costal margin and above the inferior gluteal fold, which refers to pain, muscle tension, or stiffness. The global prevalence of LBP in 2017 was 7.83%, and 577 million people were affected at any time. 1 In 2019, a systematic review of 13 studies from northern Europe, North America, and Israel reported that the prevalence of LBP ranged between 14% and 20%. 2 A systematic review and meta-analysis revealed that the lifetime prevalence of LBP was 47% in low-, lower-Fu Zhang and Songjuan Wang (shared first authorship) and Zhiyu Zhou and Shaoyu Liu (shared last authorship) contributed equally to this study.
Activation of mitophagy was considered to be a potential therapeutic strategy for intervertebral disc degeneration (IDD). There was evidence suggesting that hyaluronic acid (HA) can protect mitochondria from oxidative stress in chondrocytes, but its protective effects and mechanism in nucleus pulposus cells (NPCs) remain unclear. This study aimed to confirm the effect of HA promoting mitophagy and protecting mitochondria function in NPCs, and explore its underlying mechanism. NPCs were treated with high molecular weight HA, tert-butyl hydroperoxide (TBHP) and Cyclosporin A (CsA). Mitophagy, mitochondrial function, apoptosis, senescence and extracellular matrix (ECM) degradation were measured. Then, NPCs were transfected with C1QBP siRNA, mitophagy and mitochondrial function were tested. The therapeutic effects of HA on IDD by promoting mitophagy were assessed in bovine intervertebral disc organ culture model. The results showed that TBHP induced oxidative stress, mitochondrial dysfunction, NPCs apoptosis, senescence and ECM degradation. Treated by HA, mitophagy was activated, concomitantly, mitochondrial dysfunction, apoptosis, senescence and ECM degradation were ameliorated. Mitophagy inhibition by CsA partially eliminated the protective effects of HA against oxidative stress. After transfected with C1QBP siRNA to reduce the expression of C1QBP in NPCs, the effect of HA promoting mitophagy was inhibited and the protective effect of HA against oxidative stress was weaken. Additionally, HA alleviated NPCs apoptosis and ECM degradation in bovine intervertebral disc organ culture model. These findings suggest that HA can protect mitochondrial function through activation of mitophagy in NPCs and ameliorate IDD. Furthermore, C1QBP is involved in HA promoting mitophagy and protecting NPCs from oxidative stress. Taken together, our results provide substantial evidence for the clinical applications of HA in the prevention and treatment of IDD.
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