Search

Intervertebral disc degeneration (IDD) disease has been considered as the main cause of low back pain (LBP), which is a very common symptom and the leading cause of disability worldwide today. The pathological mechanism of IDD remains quite complicated, and genetic, developmental, biochemical, and biomechanical factors all contribute to the development of the disease. There exists no effective, non‐surgical treatment for IDD nowadays, which is largely related to the lack of knowledge of the specific mechanisms of IDD, and the lack of effective specific targets. Recently, non‐coding RNA, including miRNA, has been recognized as an important regulator of gene expression. Current studies on the effects of miRNA in IDD have confirmed that a variety of miRNAs play a crucial role in the process of IDD via nucleus pulposus cells (NPC) apoptosis, abnormal proliferation, inflammatory factors, the extracellular matrix (ECM) degradation, and annulus fibrosus (AF) degeneration. In the past 10 years, research on miRNA has been quite active in IDD. This review summarizes the current research progression of miRNA in the IDD and puts forward some prospects and challenges on non‐surgical treatment for IDD. [ABSTRACT FROM AUTHOR]

Low back pain (LBP) is one of the most common health problems in people's lives, which brings a massive burden to clinicians, and the leading cause of LBP is intervertebral disc degeneration (IDD). IDD is mainly caused by factors such as aging, mechanical stress, and lack of nutrition. The pathological mechanism of IDD is very complex, involving inflammatory response, cell metabolism disorder, and so on. Unfortunately, in the current treatment of IDD, only relieving symptoms as the primary means of relieving a patient's pain cannot effectively inhibit or reverse the progression of IDD. Tumor necrosis factor-α (TNF-α) is a multifunctional pro-inflammatory factor involved in many diseases' pathological processes. With the in-depth study of the pathological mechanism of IDD, more and more evidence has shown that TNF-α is an essential activator of IDD, which is related to the metabolic disorder, inflammatory responses, apoptosis, and other pathological processes of extracellular dissociation in the intervertebral disc. Therefore, anti-TNF-α therapy is an effective therapeutic target for alleviating IDD, especially in inhibiting extracellular matrix degradation and reducing inflammatory responses. This article reviews the pathological role of TNF-α in IDD and the latest research progress of TNF-α inhibitors in treating IDD. • Summary of TNF-α and pathological mechanisms of Intervertebral Disc Degeneration and new research. • Discuss the relationship between TNF-α in intervertebral disc degeneration, NP cell apoptosis, pyroptosis and autophagy. • The figures in the article should give scholars who are new to this field a direct understanding of the mechanism. • It may be helpful to treat intervertebral disc degeneration with TNF-α inhibitors. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration (IDD) is the leading cause of low back pain (LBP) and disability in the elderly, imposing significant public health and economic burden worldwide. Meanwhile, the pathological mechanisms of IDD remain complicated, and treatment strategy to reverse IDD is primarily due to the unclear specific mechanisms of IDD and the lack of particular effective targets. Interleukin-1β (IL-1β), one of the most important members of the IL-1 family, can induce solid pro-inflammatory activity by stimulating the secretion of various pro-inflammatory mediators and is considered the key to IDD mediator. However, in recent years, IL-1β is considered to be able to regulate IVD cell death in many ways, such as apoptosis, pyroptosis, ferroptosis, and so on. At the same time, numerous studies on IL-1β inhibitors suggest that inhibition of IL-1β may be a promising biological therapy for IDD. Many IL-1β inhibitors have been investigated through various pathogenic biological mechanisms, including inhibiting inflammatory processes, regulating ECM degradation, and more. Therefore, anti-IL-1β therapy may have the effect of alleviating disc degeneration. This article mainly reviews the mechanisms and functions of IL-1β in IDD and investigates advances in IL-1β inhibition as a promising biotherapeutic approach for disc degeneration. • The current article reviews the mechanisms and functions of IL-1β in IDD and investigates advances in IL-1β inhibition as a promising biotherapeutic approach for disc degeneration. We demonstrate function of IL-1β from different aspects, such as inflammatory responses, ECM metabolism, cell senescence, cell apoptosis, pyroptosis, and ferroptosis, oxidative stress, angiogenesis and neoinnervation in IDD. It is suitable for the audience of Experimental Gerontology, as IDD is a condition affecting the elderly. • This article could provide a valuable resource for researchers and clinicians seeking to better understand the role of IL-1β in IDD and explore potential therapeutic targets. • We provide a comprehensive review of the involvement of IL-1β in intervertebral disc degeneration (IVDD) and its potential as a therapeutic target. However, the article would benefit from a more detailed discussion on the differences between animal models and human in vivo experiments, as well as the potential limitations and challenges in translating these findings to human subjects. • We have presented several studies that show the promising effects of IL-1β inhibition in vitro and in animal models. However, the safety, reliability, and effectiveness of such treatments in humans remain uncertain. The article would benefit from a discussion of the challenges in conducting clinical trials for these treatments and the need for more extensive clinical studies in the future. • While we acknowledge the difficulty of studying intervertebral disc (IVD) tissue homeostasis, the review would benefit from a more in-depth exploration of the inflammatory process during IDD and its implications for the development of IL-1β-centered therapies. This may include a discussion of the role of inflammation in maintaining homeostasis and the potential risks of completely suppressing IL-1β-induced inflammation. • The article discusses the potential for IL-1β-centered therapy to restore homeostasis in the intervertebral disc. However, it would be beneficial for researchers and clinicians to provide more information on the current state of research in this area, including any promising drug candidates or novel approaches to treatment. [ABSTRACT FROM AUTHOR]