Intervertebral disc degeneration (IDD) is a common clinical degenerative disease of the spine. A series of factors, such as inflammation, oxidative stress and mechanical stress, promote degradation of the extracellular matrix (ECM) of the intervertebral discs (IVD), leading to dysfunction and structural destruction of the IVD. Nuclear factor‐κB (NF‐κB) transcription factor has long been regarded as a pathogenic factor of IDD. Therefore, NF‐κB may be an ideal therapeutic target for IDD. As NF‐κB is a multifunctional functional transcription factor with roles in a variety of biological processes, a comprehensive understanding of the function and regulatory mechanism of NF‐κB in IDD pathology will be useful for the development of targeted therapeutic strategies for IDD, which can prevent the progression of IDD and reduce potential risks. This review discusses the role of the NF‐κB signalling pathway in the nucleus pulposus (NP) in the process of IDD to understand pathological NP degeneration further and provide potential therapeutic targets that may interfere with NF‐κB signalling for IDD therapy.

This study aimed to find potential diagnostic markers for osteoarthritis (OA) and analyze the role of immune cells infiltration in this pathology. We used OA datasets from the Gene Expression Omnibus database. First, R software was used to identify differentially expressed genes (DEGs) and perform functional correlation analysis. Then least absolute shrinkage and selection operator (LASSO) logistic regression and support vector machine-recursive feature elimination algorithms were used to screen and verify the diagnostic markers of OA. Finally, CIBERSORT was used to evaluate the infiltration of immune cells in OA tissues, and the correlation between diagnostic markers and infiltrating immune cells was analyzed. A total of 458 DEGs were screened in this study. GRB10 and E2F3 (AUC = 0.962) were identified as diagnostic markers of OA. Immune cell infiltration analysis found that resting mast cells, T regulatory cells, CD4 memory resting T cells, activated NK cells, and eosinophils may be involved in the OA process. In addition, GRB10 was correlated with NK resting cells, naive CD4 + T cells, and M1 macrophages, while E2F3 was correlated with resting mast cells. In conclusion, GRB10 and E2F3 can be used as diagnostic markers of osteoarthritis, and immune cell infiltration plays an important role in the occurrence and progression of OA.

Intervertebral disc degeneration (IDD), an important cause of chronic low back pain (LBP), is considered the pathological basis for various spinal degenerative diseases. A series of factors, including inflammatory response, oxidative stress, autophagy, abnormal mechanical stress, nutritional deficiency, and genetics, lead to reduced extracellular matrix (ECM) synthesis by intervertebral disc (IVD) cells and accelerate IDD progression. Mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase that plays a vital role in diverse degenerative diseases. Recent studies have shown that mTOR signalling is involved in the regulation of autophagy, oxidative stress, inflammatory responses, ECM homeostasis, cellular senescence, and apoptosis in IVD cells. Accordingly, we reviewed the mechanism of mTOR signalling in the pathogenesis of IDD to provide innovative ideas for future research and IDD treatment.

Intervertebral disc degeneration (IDD) is a major cause of lower back pain. The pathophysiological development of IDD is closely related to the stimulation of various stressors, including proinflammatory cytokines, abnormal mechanical stress, oxidative stress, metabolic abnormalities, and DNA damage, among others. These factors prevent normal intervertebral disc (IVD) development, reduce the number of IVD cells, and induce senescence and apoptosis. Stress-activated protein kinases (SAPKs), particularly, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), control cell signaling in response to cellular stress. Previous studies have shown that these proteins are highly expressed in degenerated IVD tissues and are involved in complex biological signal-regulated processes. Therefore, we summarize the research reports on IDD related to JNK and p38 MAPK. Their structure, function, and signal regulation mechanisms are comprehensively and systematically described and potential therapeutic targets are proposed. This work could provide a reference for future research and help improve molecular therapeutic strategies for IDD.

S100A6, also known as calcyclin, is a low-molecular-weight Ca²⁺-binding protein from the S100 family that contains two EF-hands. S100A6 is expressed in a variety of mammalian cells and tissues. It is also expressed in lung, colorectal, pancreatic, and liver cancers, as well as other cancers such as melanoma. S100A6 has many molecular functions related to cell proliferation, the cell cycle, cell differentiation, and the cytoskeleton. It is not only involved in tumor invasion, proliferation, and migration, but also the pathogenesis of other non-neoplastic diseases. In this review, we focus on the molecular mechanisms and potential therapeutic targets of S100A6 in tumors, nervous system diseases, leukemia, endometriosis, cardiovascular disease, osteoarthritis, and other related diseases.