Researchers have develped a microbe–gut–cartilage axis-on-a-chip platform to investigate the pathogenic mechanisms underlying osteoarthritis.
Spatial transcriptomics identifies neutrophil–epithelial niches that promote kidney injury in ANCA-associated glomerulonephritis.
Arthritis is characterized by pain and inflammation of the joints, with the most common forms being osteoarthritis (OA) and rheumatoid arthritis (RA). These conditions affect a sizeable portion of the adult population, creating substantial health and socioeconomic burdens. Dysregulated inflammatory pathways contribute to arthritis and represent important targets for current and emerging therapies. Symptoms and cytokine levels change dynamically over time in arthritis, varying not only with disease state (such as flare-ups) but also with daily circadian rhythms. Daily fluctuations in rheumatoid arthritis symptoms are well established and parallel changes in inflammatory mediators, whereas osteoarthritis seems to exhibit more variable and patient-specific temporal patterns. Current treatments generally do not account for these biological rhythms. However, growing evidence suggests that aligning therapy with circadian fluctuations (termed ‘chronotherapy’) could improve outcomes and reduce adverse effects, although practical implementation remains challenging. Emerging synthetic biology approaches aim to enable timed drug delivery by harnessing the endogenous genetic mechanisms that regulate cellular rhythms. Together, these advances highlight opportunities for translating circadian-based therapies into clinical practice. Circadian rhythms influence processes central to arthritis pathogenesis, including inflammation, immune activity and tissue homeostasis. Harnessing these rhythms through chronotherapy and chronogenetics could improve treatment efficacy, safety and precision.
The AVP–AVPR1A–NR4A3 signalling axis mediates hypertension-associated osteoarthritis progression and represents a potential disease-modifying therapeutic target.
Findings from a genetics study identify mechanisms underlying the pathogenesis of IgA vasculitis.
