Osteoarthritis (OA), a ubiquitous degenerative joint disorder, is marked by pain and disability, profoundly impacting patients' quality of life. As the population ages, the global prevalence of OA is escalating. Omics technologies have become instrumental in investigating complex diseases like OA, offering comprehensive insights into its pathogenesis and progression by uncovering disease-specific alterations across genomics, transcriptomics, proteomics, and metabolomics levels. In this review, we systematically analyzed and summarized the application and recent achievements of omics technologies in OA research by scouring relevant literature in databases such as PubMed. These studies have shed light on new potential therapeutic targets and biomarkers, charting fresh avenues for OA diagnosis and treatment. Furthermore, in our discussion, we highlighted the immense potential of spatial omics technologies in unraveling the molecular mechanisms of OA and in the development of novel therapeutic strategies, proposing future research directions and challenges. Collectively, this study encapsulates the pivotal advances in current OA research and prospects for future investigation, providing invaluable references for a deeper understanding and treatment of OA. This review aims to synthesize the recent progress of omics technologies in the realm of OA, aspiring to furnish theoretical foundations and research orientations for more profound studies of OA in the future.

Gouty nephropathy (GN) is a metabolic disease with persistently elevated blood uric acid levels. The main manifestations of GN are crystalline kidney stones, chronic interstitial nephritis, and renal fibrosis. Understanding the mechanism of the occurrence and development of GN is crucial to the development of new drugs for prevention and treatment of GN. Currently, most studies exploring the pathogenesis of GN are primarily based on animal and cell models. Numerous studies have shown that inflammation, oxidative stress, and programmed cell death mediated by uric acid and sodium urate are involved in the pathogenesis of GN. In this article, we first review the mechanisms underlying the abnormal intrinsic immune activation and programmed cell death in GN and then describe the characteristics and methods used to develop animal and cell models of GN caused by elevated uric acid and deposited sodium urate crystals. Finally, we propose potential animal models for GN caused by abnormally high uric acid levels, thereby provide a reference for further investigating the methods and mechanisms of GN and developing better prevention and treatment strategies.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by persistent synovitis, progressive joint destruction, and diverse extra-articular complications. Increasing evidence indicates that RA pathogenesis is not driven by isolated inflammatory events, but by a tightly interconnected network involving immune dysregulation, metabolic reprogramming, and aberrant mechanotransduction. This review synthesizes recent advances in these three pathogenic dimensions and proposes an integrated framework for understanding RA as a systemic, self-reinforcing disease process. We highlight how inflammatory circuits, particularly the IL-6/STAT3 and TNF-α/NF-κB axes, interact with autoantibody- and neutrophil extracellular trap-mediated immune propagation beyond the synovium. We further discuss how glycolytic rewiring, succinate accumulation, and microbiota-derived metabolites amplify inflammatory signaling and tissue remodeling. In parallel, altered extracellular matrix stiffness and activation of the integrin-FAK-YAP/TAZ pathway sustain pathogenic fibroblast behavior through mechano-epigenetic coupling. Collectively, these pathways form a feed-forward loop that links local synovial inflammation with systemic organ involvement. A systems-level understanding of these interactions may provide a stronger foundation for biomarker-guided stratification and the development of multi-target, mechanism-based therapeutic strategies in RA.

Gouty arthritis (GA), a metabolic and immunologic disease, primarily affects joints. Dysbiosis of intestinal flora is an important cause of GA. The metabolic disorders of intestinal flora leading to GA and immune disorders might play an important role in patients with hyperuricemia and established GA. However, the exact mechanisms, through which the dysbiosis of intestinal flora causes the development of GA, are not fully understood yet. Moreover, several therapies commonly used to treat GA might alter the intestinal flora, suggesting that modulation of the intestinal flora might help prevent or treat GA. Therefore, a better understanding of the changes in the intestinal flora of GA patients might facilitate the discovery of new diagnostic and therapeutic approaches. The current review article discusses the effects of intestinal flora dysbiosis on the pathogenesis of GA and the cross-regulatory effects between gut flora and drugs for treating GA. This article also highlights the modulatory effects of gut flora by traditional Chinese medicine (TCM) to lower uric acid levels and relieve joint pain as well as provides a summary and outlook, which might help guide future research efforts.

Uric acid has complex bidirectional effects on human physiology and disease, influenced by its antioxidant capacity, metabolic regulatory roles, and pro-inflammatory properties, all of which are highly context-dependent. In this review, we synthesize recent advancements related to the continuum from soluble uric acid (SUA) to amorphous monosodium urate (AMSU) and, ultimately, to crystalline monosodium urate (MSU). We propose that AMSU may act as a transitional intermediate that connects the soluble and crystalline states. Notably, AMSU may serve as a buffering stage between crystallization and inflammatory activation, providing a conceptual bridge between urate phase transitions and immune–metabolic signaling. Building on this idea, we establish a framework that links urate state dynamics with immune-metabolic pathways and disease progression. We systematically summarize the physiological roles of SUA in maintaining redox homeostasis and regulating metabolism, and we examine how sustained hyperuricemia contributes to chronic organ damage through impaired autophagy and metabolic inflammation. Additionally, we outline how the formation of MSU crystals triggers acute inflammatory responses via the TLR–NLRP3 two-signal model. Subsequent processes, such as neutrophil extracellular traps formation and macrophage polarization, drive chronic tissue remodeling and progressive pathology. Finally, we connect these mechanistic insights to both established and emerging therapeutic strategies, emphasizing the potential value of stage-specific and mechanism-oriented interventions. By conceptualizing uric acid biology as a dynamic, multi-state process, this review offers an integrated perspective on hyperuricemia-associated diseases and suggests directions for future targeted therapeutic research.

Background: The exact pathogenesis of gouty arthritis (GA) is unclear. However, it is believed that GA is characterized by recurrent episodes and a self-limiting nature. During episodes, the disease primarily manifests locally, making local omics research particularly relevant. Objective: Based on the local proteomic analysis of GA patients during the chronic phase (with tophi) and acute phase (with joint cavity effusion), this study systematically screened for inflammation-related differentially expressed proteins to provide specific biomarkers and potential intervention targets for disease prevention and treatment. Methods: Through a cross-sectional study, the baseline data were collected from the GA patients with chronic phase (with tophi) and acute phase (with joint cavity effusion)(n = 100 per group). Five cases were randomly selected from each group for local proteomics analysis to determine the biological functions and enriched signaling pathways of differentially expressed proteins. Based on the differential results, 30 additional cases were randomly selected from each group for validation using Western blot analysis. Results: The quantitative proteomics analysis identified a total of 810 differentially expressed proteins between the two groups, including 548 upregulated and 262 downregulated proteins. The GO and KEGG pathway enrichment analysis showed that the differential proteins were associated with ferroptosis. Ultimately, three ferroptosis-related differential proteins, including glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), arachidonate and 15-lipoxygenase (ALOX15) were identified in GA patients. The differential expression of these proteins was validated using Western blot, showing statistically significant differences ( P < 0.05). Conclusions: The comprehensive analysis of proteomics and Western blot validation experiments showed that local lesions in the chronic phase of GA exhibited increased expression levels of GPX4 and FTH1, while local lesions in the acute phase of GA exhibited increased expression of ALOX15. Therefore, it was speculated that ferroptosis-inhibiting factors in the chronic phase of GA might participate in the chronic progression of the disease by limiting the toxicity of free iron. In the acute phase of GA, ferroptosis-promoting factors were activated in the joint microenvironment. This study revealed the differential expression of ferroptosis-related proteins at different stages of GA, providing a theoretical basis for developing GA staging and treatment strategies based on ferroptosis regulation.