Single-cell sequencing technology provides a high-resolution perspective for the precision diagnosis and treatment of chronic myeloid leukemia (CML). Cellular and molecular heterogeneity in CML is closely associated with tyrosine kinase inhibitor resistance, residual disease, and disease progression. However, the averaged signals generated by conventional bulk sequencing limit the identification of minor resistant clones, state-dependent leukemia stem cell (LSC) programs, and complex microenvironmental interactions. This review summarizes frontier applications of single-cell RNA sequencing and related single-cell omics technologies in CML, including molecular mechanism analysis, tumor microenvironment profiling, resistance mechanism exploration, biomarker discovery, and the translation of these findings into risk stratification, treatment monitoring, and individualized therapeutic strategies. By integrating recent global research findings, this review discusses the value of single-cell technology in revealing the functional heterogeneity of LSCs and provides a balanced perspective on the future integration of spatial multi-omics, artificial intelligence-assisted analysis, and clinical decision systems. The aim is to clarify how CML diagnosis and treatment may move from empiric disease monitoring toward a more precise, single-cell-informed model while acknowledging current technical, economic, regulatory, and validation barriers.

Atherosclerosis (AS) is a chronic cardiovascular disease. Traditional lipid-lowering treatments have not fully reduced the risk of disease onset in high-risk patients. This review provides a systematic overview of immune microenvironment remodeling and the mechanisms of pyroptosis during the onset and progression of atherosclerosis. Studies have shown that AS is not only related to abnormal lipid metabolism, but also closely associated with inflammatory responses, activation of immune cells, and programmed cell death. Immune cells, including macrophages, T cells, and B cells, play key roles in plaque formation, progression, and rupture. At the same time, NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis exacerbates plaque instability by promoting the release of inflammatory mediators, including Interleukin-1β (IL-1β) and interleukin-18 (IL-18), We further summarize emerging therapeutic strategies targeting immune regulation and pyroptosis pathways, including NLRP3 inhibitors, cytokine-targeted agents, and nano-drug delivery systems, thereby offering new perspectives for the precise treatment of AS.

Gout is an increasingly prevalent inflammatory arthritis that substantially affects quality of life and contributes to a growing public health burden. Understanding its complex network of risk factors is crucial for effective prevention and management. The emergence of large-scale cohorts, particularly the UK Biobank, has facilitated etiologic, genetic, and clinical research on gout and related urate phenotypes. By providing multidimensional lifestyle, clinical, and omics data, the UK Biobank serves as a powerful resource for dissecting the multifaceted nature of gout. Here, we provide a critical narrative review of UK Biobank-based gout research, focusing on multidimensional determinants, convergent and conflicting evidence, comorbidity networks, clinical implications, and methodological limitations and potential biases. This review aims to provide an evidence-based framework for informing gout prevention, comorbidity assessment, and future research.

Mitochondrial diseases are a group of inherited metabolic disorders caused by defects in mitochondrial DNA (mtDNA) or nuclear DNA leading to oxidative phosphorylation dysfunction. Clinical manifestations are highly heterogeneous, typically involving high-energy-demand organs (brain, muscle, heart, etc.), and curative treatments remain largely unavailable. This review examines the literature over the past decades on mitochondrial disease treatments, including traditional Cocktail therapy, target therapy, multidisciplinary management, gene therapy, mtDNA base editing, and mitochondrial replacement therapy. Although most current treatments remain symptomatic, breakthrough advances in gene therapy and base editing over recent years have brought new hope for precision medicine in mitochondrial diseases.