Osteoarthritis is a degenerative joint disorder characterized by cartilage degradation, synovial inflammation, and altered subchondral bone structure. Recent insights have identified mitochondrial dysfunction as a pivotal factor in OA pathogenesis, contributing to chondrocyte apoptosis, oxidative stress, and extracellular matrix degradation. Disruptions in mitochondrial dynamics, including impaired biogenesis, mitophagy, and metabolic shifts from oxidative phosphorylation to glycolysis, exacerbate cartilage damage by promoting the production of reactive oxygen species and matrix-degrading enzymes such as ADAMTS and MMPs. This review explores the molecular mechanisms underlying mitochondrial dysfunction in OA, emphasizing its role in cartilage homeostasis and inflammation. Furthermore, it highlights emerging therapeutic strategies targeting mitochondrial pathways, including antioxidants, mitophagy enhancers, and metabolic modulators, as potential interventions to mitigate disease progression, which offer promising avenues for advancing personalized and disease-modifying treatments in OA.

Osteoarthritis (OA) is a progressive, whole-joint disorder driven by a convergence of biomechanical stress, inflammation, metabolic dysfunction, and cellular senescence. This review integrates recent advances in our understanding of the distinct yet interconnected pathological processes affecting articular cartilage, subchondral bone, synovium, infrapatellar fat pad, menisci, ligaments, and peri-articular musculature. Emerging mechanisms, such as chondrocyte ferroptosis, neurovascular remodeling, and synovial-mesenchymal reprogramming, are highlighted for their roles in disease propagation and chronic pain. We critically appraise current therapeutic modalities, including evidence-based non-pharmacological strategies, pharmacologic agents, intra-articular biologics, and surgical interventions. In parallel, we explore the promise of precision medicine, multi-omics profiling, advanced imaging biomarkers, regenerative therapies, and artificial intelligence in reshaping diagnostic and treatment paradigms. This comprehensive synthesis underscores the shift toward a mechanistic, individualized approach to OA management and identifies key translational opportunities for disease modification and early intervention.

Osteosarcoma is a malignant bone tumor that is prone to metastasize early and primarily affects children and adolescents. Cell migration-inducing protein (CEMIP) plays a crucial role in the progression and malignancy of various tumor diseases, including osteosarcoma. Chitosan oligosaccharide (COS), an oligomer isolated from chitin, has been found to have significant anti-tumor activity in various cancers. This study investigates the effects of COS on CEMIP expression in osteosarcoma and explores the underlying mechanism. In present study, in vitro experiments were conducted to confirm the inhibitory activity of COS on human osteosarcoma cells. Our results demonstrate that COS possesses inhibitory effects against human osteosarcoma cells and significantly suppresses CEMIP expression in vitro. Next, we studied the inhibition of the expression of CEMIP by COS and then performed bioinformatics analysis to explore the potential inhibitory mechanism of COS against signaling pathways involved in regulating CEMIP expression. Bioinformatics analysis predicted a close association between the PI3K signaling pathway and CEMIP expression and that the inhibitory effect of COS on CEMIP expression may be related to PI3K signaling pathway regulation. The results of this study show that COS treatment significantly inhibits CEMIP expression and the PI3K/AKT/mTOR signaling pathway, as observed both in vitro and in vivo. This study demonstrates that COS could inhibit the expression of CEMIP, which is closely related to osteosarcoma malignancy. This inhibitory effect may be attributed to the inhibition of the PI3K/AKT/mTOR signaling pathway in vitro and in vivo.

Postoperative nausea and vomiting (PONV) remains one of the most common and distressing adverse events after anesthesia and surgery, with important effects on patient comfort, recovery quality, discharge readiness, and healthcare resource use. Although advances in anesthetic techniques, antiemetic pharmacology, and enhanced recovery pathways have improved perioperative care, PONV continues to occur frequently because of its multifactorial pathophysiology and variable individual susceptibility. This narrative review provides a clinically oriented overview of current concepts in PONV, including epidemiology, clinical burden, neurochemical mechanisms, risk factors, prediction models, baseline risk reduction, pharmacological prophylaxis, rescue treatment, postdischarge care and future perspectives. PONV results from complex interactions among central and peripheral emetic pathways, including gastrointestinal vagal afferents, the chemoreceptor trigger zone, vestibular input, higher cortical and limbic modulation, and multiple neurotransmitter systems such as serotonin, dopamine, histamine, acetylcholine, substance P, and opioid-mediated signaling. Structured risk assessment, particularly using simplified prediction tools such as the Apfel score, remains essential for guiding individualized prophylaxis. Preventive strategies should combine reduction of modifiable perioperative risk factors with appropriate multimodal antiemetic therapy. Key interventions include minimizing exposure to volatile anesthetics and nitrous oxide when suitable, using opioid-sparing analgesia, optimizing hydration and fasting practices, and integrating regional or neuraxial techniques when appropriate. Pharmacological management relies on agents targeting different receptor systems, including 5-HT3 receptor antagonists, dopamine receptor antagonists, neurokinin-1 receptor antagonists, glucocorticoids, anticholinergics, and antihistamines. Future research should improve prediction accuracy, clarify optimal prophylactic combinations, strengthen guideline implementation, evaluate postdischarge symptoms, and explore artificial intelligence-assisted individualized prevention. A comprehensive, risk-based, and patient-centered approach remains central to reducing the burden of PONV.