Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a chronic inflammation of the gastrointestinal tract with unknown etiology. The cause of IBD is widely considered multifactorial, with prevailing hypotheses suggesting that the microbiome and various environmental factors contribute to inappropriate activation of the mucosal immune system in genetically susceptible individuals. Although the incidence of IBD has stabilized in Western countries, it is rapidly increasing in newly industrialized countries, particularly China, making IBD a global disease. Significant changes in multiple biomarkers before IBD diagnosis during the preclinical phase provide opportunities for earlier diagnosis and intervention. Advances in technology have driven the development of telemonitoring tools, such as home-testing kits for fecal calprotectin, serum cytokines, and therapeutic drug concentrations, as well as wearable devices for testing sweat cytokines and heart rate variability. These tools enable real-time disease activity assessment and timely treatment strategy adjustments. A wide range of novel drugs for IBD, including interleukin-23 inhibitors (mirikizumab, risankizumab, and guselkumab) and small-molecule drugs (etrasimod and upadacitinib), have been introduced in the past few years. Despite these advancements, approximately one-third of patients remain primary non-responders to the initial treatment, and half eventually lose response over time. Precision medicine integrating multi-omics data, advanced combination therapy, and complementary approaches, including stem cell transplantation, psychological therapies, neuromodulation, and gut microbiome modulation therapy, may offer solutions to break through the therapeutic ceiling.
Humans ; Inflammatory Bowel Diseases/therapy*

Objective To explore the correlation between HIF-1α expression and RANKL/OPG pathway activation of fibroblast-like synoviocytes(FLSs)induced by Ti particles in aseptic loosening interfacial membrane. Method FLSs were extracted from the synovial tissue collected in surgeries and then co-cultured with Ti particles. QRT-PCR and Western blotting were conducted to measure the mRNA and protein expression of RANKL ,OPG and HIF-1αin FLSs at different concentration and time. Results Genes and protein expression levels of RANKL/OPG and HIF-1α were up-regulated with the increase of concentration of Ti particles. Expression of HIF-1α gene and protein increased time-dependently;the mRNA and protein expression of RANKL/OPG increased firstly and then declined alongside the increase of HIF-1αexpression. Conclusions Ti particles induce the up-regulation of HIF-1α expression and activate RANKL/OPG pathway. Up-regulation of HIF-1α may suppress the activation of RANKL/OPG pathway in FLSs of the interfacial membrane induced by Ti particles.