Hyperuricaemia (HUA) is a metabolic disorder resulting from the dysregulation of purine metabolism. It is closely associated with gout and various metabolic syndromes, representing an increasing global public health challenge. Current treatment approaches for HUA and gout generally involve the lifelong administration of urate-lowering agents to maintain optimal serum urate concentrations. However, poor patient adherence, often due to potential hepatorenal toxicity, frequently leads to disease relapse. Recent evidence indicates that the gut microbiota plays a significant role in maintaining urate homeostasis through multiple mechanisms, including the modulation of purine metabolism, urate catabolism and excretion, regulation of inflammatory responses, and preservation of intestinal barrier integrity. These findings highlight the gut microbiota as a promising novel therapeutic target. This review synthesizes recent progress in three key areas: (1) the relationship between the gut microbiota and HUA; (2) microbial mechanisms underlying urate-lowering effects, such as microbial purine and urate metabolism, regulation of urate transporters like ABCG2, and production of anti-inflammatory metabolites; and (3) microbiota-based therapeutic interventions, including probiotics, engineered bacterial strains, fecal microbiota transplantation, and pharmabiotic strategies. Additionally, we explore the translational potential of microbiota modulation in clinical settings and outline directions for future research. By integrating mechanistic understanding with therapeutic innovation, this review offers researchers and clinicians a comprehensive framework for advancing microbiota-targeted approaches in the management of hyperuricaemia.

Propofol is widely used as an intravenous anesthetic in clinical practice. Previous studies have indicated that propofol induces apoptosis in neurons. Brain-derived neurotrophic factor (BDNF), a neurotrophic factor, is associated with neuronal apoptosis. BDNF-AS, a relatively conserved long non-coding RNA, can reverse the transcription of BDNF. This study aimed to investigate the involvement of BDNF-AS in propofol-induced apoptosis in HT22 cells. HT22 cells were treated with various concentrations of propofol at different time points. BDNF-AS was silenced using BDNF-AS-targeting siRNA. TrkB was antagonized by the TrkB inhibitor, ANA-12. Flow cytometry, quantitative reverse-transcription PCR, and western blotting were performed to analyze apoptosis and the expression of genes and proteins, respectively. In propofol-treated HT22 cells, BDNF-AS was upregulated, and BDNF was downregulated in a time- and dose-dependent manner. BDNF-AS downregulation mediated by siRNA mitigated apoptosis, upregulated the expression of Bcl-2, and downregulated the expression of Bax and caspase-3, 7, and 9. ANA-12 downregulated the expression of Bcl-2, upregulated the expression of Bax and caspase-3, 7, and 9, and increased apoptosis. Our study implied that inhibition of BDNF-AS can decrease propofol-induced apoptosis by activating the BDNF/TrkB pathway. Thus, the BDNF-AS-BDNF/TrkB signaling pathway may be a valuable target for treating propofol-induced neurotoxicity.

Coronary atherosclerosis, driven by the interplay of lipid metabolic derangements and chronic inflammation, constitutes the pathological basis of atherosclerotic cardiovascular disease and has emerged as the leading cause of mortality among Chinese residents. In patients with acute coronary syndrome, subsequent events may arise from initially nonculprit coronary lesions that appear angiographically mild. Invasive coronary angiography, the conventional diagnostic reference standard, is inherently invasive and incapable of characterizing plaque biological properties. Meanwhile, traditional risk factors only enable crude risk stratification, resulting in a critical shortage of precise early clinical screening modalities. Multi-omics technologies enable comprehensive molecular profiling of the human organism and effectively address the limitations of conventional detection approaches. Nevertheless, existing investigations remain largely confined to single-omics analyses; candidate biomarkers lack validation in large independent cohorts, and substantial bottlenecks persist in clinical translation. This review evaluates the respective advantages and limitations of genomics, epigenomics, transcriptomics, proteomics, metabolomics, lipidomics, and gut metagenomics in coronary atherosclerosis research. It elucidates the scientific value of integrated multi-omics analysis in dissecting pathogenic regulatory networks, unraveling gut-heart axis mechanisms, and identifying targets for precision therapy. Furthermore, it summarizes cutting-edge technological advances including single-cell multi-omics, spatial multi-omics, liquid biopsy, and AI-powered multi-omics integration, and compiles multi-omics risk prediction models developed on the basis of large-scale population cohorts. By bridging genetic susceptibility, cellular remodeling, peripheral molecular signatures, and plaque phenotypes, multi-omics integration can underpin early risk warning for high-risk populations, plaque subtyping, and therapeutic efficacy monitoring. Looking ahead, the establishment of standardized, multicenter prospective cohorts and the application of Mendelian randomization to infer causal relationships will be pivotal. These efforts are essential to translate multi-omics into a practical framework for comprehensive precision medicine across the entire continuum of coronary atherosclerosis.