Knee osteoarthritis (KOA) is a common chronic disease in orthopedics, which brings great pain to patients' life and spirit. Therefore, it is necessary to elucidate the pathogenesis of KOA. The pathophysiology of KOA has been linked to numerous factors, including oxidative stress, apoptosis, cellular senescence, mitochondrial dysfunction, and inflammatory factors. Cellular senescence has grown in importance as a topic of study for age-related illnesses recently. KOA has also been discovered to be closely related to human aging, a process in which chondrocyte senescence may be crucial. Numerous researches have looked at the pathogenesis of KOA from the perspectives of mechanical stress abnormalities, oxidative stress, inflammatory overexpression, and mitochondrial dysfunction. Many studies have discovered that the primary pathogenesis of KOA is inflammatory overexpression and chondrocyte death brought on by an imbalance in the joint microenvironment. And abnormal mechanical stress is the initiating cause of oxidative stress, inflammation, and mitochondrial disorders. However, few findings have been reported in the literature on the relationship between these factors, especially for mechanical stress abnormalities, and chondrocyte senescence. This time, in order to better understand the pathogenesis of KOA and identify potential connections between chondrocyte senescence and these microenvironments in KOA, as well as oxidative stress, inflammatory overexpression, and mitochondrial dysfunction microenvironmental dysfunctions, we will use chondrocyte senescence as a starting point. This will allow us to develop new therapeutic approaches for KOA.

Background: Intervertebral disc degeneration (IVDD) is a leading cause of low back pain (LBP), contributing significantly to global disability and productivity loss. Its pathogenesis involves complex processes, including inflammation, cellular senescence, angiogenesis, fibrosis, neural ingrowth, and sensitization. Emerging evidence highlights macrophages as central immune regulators infiltrating degenerated discs, with macrophage polarization implicated in IVDD progression. However, the mechanisms linking macrophage polarization to IVDD pathology remain poorly elucidated.Methods: A comprehensive literature review was conducted by searching major databases (PubMed, Web of Science, and Scopus) for studies published in the last decade (2014–2024). Keywords included “intervertebral disc degeneration,” “macrophage polarization,” “inflammation,” “senescence,” and “therapeutic strategies.” Relevant articles were selected, analyzed, and synthesized to evaluate the role of macrophage polarization in IVDD.Results: Macrophage polarization dynamically influences IVDD through multiple pathways. Pro‐inflammatory M1 macrophages exacerbate disc degeneration by amplifying inflammatory cytokines (e.g., TNF‐α, IL‐1β), promoting cellular senescence, and stimulating abnormal angiogenesis and neural ingrowth. In contrast, anti‐inflammatory M2 macrophages may mitigate degeneration by suppressing inflammation and enhancing tissue repair. Therapeutic strategies targeting macrophage polarization include pharmacological agents (e.g., cytokines, small‐molecule inhibitors), biologic therapies, gene editing, and physical interventions. Challenges persist, such as incomplete understanding of polarization triggers, lack of targeted delivery systems, and limited translational success in preclinical models.Conclusion: Macrophage polarization is a pivotal regulator of IVDD pathology, offering promising therapeutic targets. Future research should focus on elucidating polarization mechanisms, optimizing spatiotemporal control of macrophage phenotypes, and developing personalized therapies. Addressing these challenges may advance innovative strategies to halt or reverse IVDD progression, ultimately improving clinical outcomes for LBP patients.

Background: To explore the mechanism of compound Hongginshen decoction in improving pulmonary fibrosis based on network pharmacology. Methods: The active components and targets of ginseng and Salvia miltiorrhiza were screened from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database. The chemical components of Rhodiola, Ophiopogon japonicus, and Dendrobium were screened using the Traditional Chinese Medicine Integrated Database (TCMID), and the target compounds were predicted by the Swisstargets method. The related target genes of pulmonary fiber (PF) were screened by the Genecards database and the National Center of Biotechnology Information (NCBI) database. The protein–protein interaction network was drawn using the string database and Cytoscape software, and the network topology was analyzed. Then, using R3.6.3 software, biological processes, molecular function, cell component enrichment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were carried out on the common targets of drugs and diseases. The network diagram of the “traditional Chinese medicine composition disease target” of Compound Hongginshen Decoction was constructed and analyzed with the software of Cytoscape 3.6.1. Results: We identified 159 active components and 2820 targets in Compound Hongginshen Decoction, and 2680 targets in pulmonary fibrosis. A total of 343 common targets were obtained by the intersection of drug targets and disease targets. protein–protein interaction protein interaction network analysis showed that PIK3CA, PIK3R1, MAPK1, SRC, AKT1, and so on may be the core targets of the compound Hongjingshen recipe in the treatment of pulmonary fibrosis. Gene Ontology (GO) enrichment analysis identified 3463 items, and KEGG pathway enrichment analysis identified 181 related signaling pathways, including the PI3K-Akt signaling pathway, HCMV pathway, Hb pathway, PGs pathway, and KSHV signaling pathway. Conclusion: Compound Hongginshen Decoction has the characteristics of a multichannel and multitargeted effect in the treatment of pulmonary fibrosis. Radix Ophiopogonis and Dendrobium officinale play a key role in the treatment of pulmonary fibrosis. The whole compound prescription may play a therapeutic role by affecting cell metabolism, being anti-inflammatory, regulating the immune system, promoting angiogenesis, and improving anaerobic metabolism.