SLC7A11 plays a pivotal role in tumour development by facilitating cystine import to enhance glutathione synthesis and counteract oxidative stress. Disulphidptosis, an emerging form of cell death observed in cells with high expression of SLC7A11 under glucose deprivation, is regulated through reduction–oxidation reactions and disulphide bond formation. This process leads to contraction and collapse of the F‐actin cytoskeleton from the plasma membrane, ultimately resulting in cellular demise. Compared to other forms of cell death, disulphidptosis exhibits distinctive characteristics and regulatory mechanisms. This mechanism provides novel insights and innovative strategies for cancer treatment while also inspiring potential therapeutic approaches for other diseases. Our review focuses on elucidating the molecular mechanism underlying disulphidptosis and its connection with the actin cytoskeleton, identifying alternative metabolic forms of cell death, as well as offering insights into disulphidptosis‐based cancer therapy. A comprehensive understanding of disulphidptosis will contribute to our knowledge about fundamental cellular homeostasis and facilitate the development of groundbreaking therapies for disease treatment.

In recent years, a growing number of studies have disclosed the substantial role of macrophages—key immune cells—in the pathological process of intervertebral disc degeneration. Researchers have categorised macrophage phenotypes into M1 and M2 polarisation, associating these polarisations with intervertebral disc degeneration. Essentially, macrophage phenotypes can be classified as either pro‐inflammatory or anti‐inflammatory. Induced by diverse factors, these distinct polarisation states exert contrary effects on disc injury and repair. Although numerous studies focus on the polarisation of macrophages and the cytokines they secrete in relation to intervertebral disc degeneration, these studies frequently neglect the relationship between the efferocytosis of macrophages and the progression of intervertebral disc degeneration. Efferocytosis is a specialised procedure in which phagocytes, such as macrophages, engulf and eliminate apoptotic cells. This process is crucial for maintaining tissue homeostasis and resolving inflammation. By effectively clearing these dying cells, efferocytosis helps prevent the release of potentially detrimental cellular contents, thereby facilitating healing and the resolution of inflammation. Simultaneously, macrophages digest the engulfed cell debris and release various cytokines that participate in tissue self‐repair. Therefore, this article presents an overview of the molecular mechanisms connecting macrophages and their efferocytosis activity to intervertebral disc degeneration, explores new directions for the utilisation of macrophages in the treatment of intervertebral disc degeneration, and discusses the future prospects for the development of therapeutic targets.

Background: Polyamide 6 microplastics (PA6-MPs), as emerging environmental pollutants, have attracted increasing attention due to their potential health risks. Their accumulation in human intervertebral disc tissue (86.4 particles/g) suggests a possible role in intervertebral disc degeneration (IVDD). However, direct evidence and mechanistic understanding remain limited. This study aimed to investigate the association between PA6-MPs exposure and IVDD, based on the hypothesis that PA6-MPs promote IVDD progression by targeting key regulatory molecules and disrupting cellular homeostasis. Methods: Potential PA6-related targets were predicted using multiple public databases, and IVDD-related differentially expressed genes were obtained from the GEO database. Overlapping targets were identified and analyzed through protein–protein interaction (PPI) network construction, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to screen core targets and pathways. Molecular docking was performed to evaluate PA6–protein binding. In vitro validation was conducted using primary human nucleus pulposus cells exposed to PA6-MPs, with cell viability, proliferation, and phenotypic changes assessed by CCK-8, EdU, live/dead staining, and immunofluorescence (IF). Results: A total of 222 PA6-related targets and 1035 IVDD-associated genes were identified, yielding 10 overlapping targets. Four core targets, including NR3C1 and HDAC1, were selected. Molecular docking and experiments demonstrated stable binding and concentration-dependent inhibition of cell viability and proliferation. Conclusion: PA6-MPs may accelerate IVDD progression in a concentration-dependent manner by targeting key molecules and perturbing inflammatory homeostasis. These findings link environmental exposure to IVDD and provide a basis for future risk assessment and targeted intervention strategies.