Despite the authoritative framework for hormone therapy provided by the 2025 European Society of Endocrinology Clinical Practice Guidelines for the Assessment and Management of Menopause and Perimenopause, there remains a notable absence of diagnostic and therapeutic protocols for sleep disorders. Given that sleep disorders affect 50% to 55% of the perimenopausal population, they constitute an independent risk factor for severe adverse health outcomes. Leveraging landmark data from the 2024 Study of Women's Health Across the Nation (SWAN), persistent insomnia symptoms are associated with a 71% increased incidence of cardiovascular events, independent of vasomotor symptoms. Furthermore, the unique female phenotype of obstructive sleep apnoea (OSA) frequently leads to misdiagnosis in endocrine clinical practice. The"tipping point" of late perimenopause presents a critical window for intervention. A more comprehensive approach-combining mandatory screening with tiered sleep interventions-can enhance daytime functioning, prevent misdiagnosis, and reduce long-term cardiovascular disease incidence. Future guidelines should explicitly address this intersection to support more personalised care for middle-aged women.

The immune and inflammatory responses following ischemic stroke involve aberrant DNA exposure, immunothrombosis, and innate immune activation. Post-stroke, damage-associated DNA signals from multiple sources may activate DNA-sensing pathways; however, how DNA from distinct sources links peripheral immune activation with inflammatory amplification within the brain remains incompletely understood. Among these, neutrophil extracellular traps (NETs), as DNA-rich extracellular structures, may represent a potential link connecting vascular inflammation, immunothrombosis, and intracerebral DNA sensing. The cyclic GMP-AMP synthase–stimulator of interferon genes (cGAS–STING) pathway, a key DNA-sensing axis, mediates distinct inflammatory and stress responses across various stroke-associated cell types. This review summarizes the mechanisms of DNA recognition, NET-mediated immunothrombosis, and neuroinflammatory damage, as well as the functional characteristics of cGAS–STING signaling in different cell types. Based on current evidence, we propose a potential NETs–cGAS–STING inflammatory amplification framework: NET-derived DNA may contribute to DNA-sensing activation within the ischemic brain and promote microglial inflammatory responses, while the resulting inflammatory factors and chemotactic signals may further promote neutrophil recruitment and secondary NET formation, thereby potentially creating a feed-forward loop linking peripheral immune activation with neuroinflammation. We further discuss the spatiotemporal heterogeneity of this axis, therapeutic targets, and challenges for clinical translation. Overall, the NETs–cGAS–STING framework provides an integrated conceptual perspective for understanding the intercellular interactions underlying DNA recognition and the sustained amplification of inflammation following stroke, and offers insights into future precision immune interventions tailored to disease stage, lesion characteristics, and cell-specific responses.

Although Helicobacter pylori (H. pylori) has been hypothesized to modulate immune responses in the context of asthma, recent epidemiological evidence has yielded contradictory results. This updated meta-analysis systematically re-evaluates the association between H. pylori infection and asthma risk to clarify these discrepancies. A systematic review and meta-analysis were conducted following PRISMA 2020 guidelines. We systematically searched PubMed, Web of Science, Cochrane Library, and Embase up to February 2026 to identify eligible observational studies. To evaluate the risk association, pooled odds ratios (ORs) and hazard ratios (HRs) with 95

Diabetes is a significant global public health issue, and atherosclerosis serves as the primary pathological basis for the occurrence and progression of cardiovascular and cerebrovascular events. Studies have shown that hyperglycemia can promote the occurrence and progression of atherosclerosis by damaging vascular endothelial cells, macrophages, and vascular smooth muscle cells. In recent years, Chinese herbal medicines and their active ingredients have demonstrated unique advantages in preventing and treating high-glucose-induced vascular cell damage. Their mechanisms of action primarily encompass two aspects: firstly, regulating blood glucose through multiple pathways such as modulating the insulin signaling pathway, enhancing peripheral glucose uptake and utilization, and delaying intestinal carbohydrate absorption; secondly, intervening in key pathological processes such as high-glucose-induced vascular cell inflammation, cell death, phenotypic transformation, and metabolic reprogramming. This, in turn, slows down the progression of diabetes-related atherosclerosis. This article systematically elucidates the molecular mechanisms underlying hyperglycemia-induced damage to vascular endothelial cells, macrophages, and vascular smooth muscle cells. It also summarizes the protective mechanisms of Chinese herbal medicine active ingredients (albiflorin, salvianolic acid B, scutellarin, vitexin, hydroxysafflor yellow A, ginsenoside Rb1, maslinic acid, paeonol, citronellal, matrine, Panax notoginseng saponins, astragalus polysaccharides, 6-gingerol, and sodium tanshinone IIA sulfonate) and traditional Chinese medicine compounds (buyang huanwu decoction, guanxining tablets, and fufang zhenzhu tiaozhi) against vascular endothelial cells, macrophages, and vascular smooth muscle cells. The aim is to provide a theoretical basis for the prevention and treatment of diabetes-related atherosclerosis, as well as the development of related therapeutic drugs.

Ischemic stroke remains one of the leading causes of death and long-term disability worldwide. The current standard-of-care therapies-intravenous thrombolysis and mechanical thrombectomy-restore cerebral blood flow but may paradoxically evoke cerebral ischemia-reperfusion injury. Recent studies have revealed that ferroptosis, a form of regulated cell death dependent on iron, plays a pivotal role in cerebral ischaemia-reperfusion injury. Traditional Chinese herbal formulas and their bioactive components can modulate ferroptosis, thereby mitigating brain damage induced by ischemia-reperfusion. This article reviews the molecular mechanisms of ferroptosis and its pathophysiological roles in cerebral ischaemia-reperfusion. It focuses particularly on the key mechanisms underlying the therapeutic effects of Chinese herbal medicines in targeting ferroptosis. The aim is to provide a theoretical basis for developing novel therapeutics.

Hyperuricemia is a significant risk factor for gout, cardiovascular disease, and chronic kidney disease, and its global prevalence has continued to rise. Genome-wide association studies (GWAS) have made significant advances in elucidating the genetic basis of serum uric acid levels, identifying key loci such as SLC2A9, ABCG2, SLC22A12, GCKR, and HNF4A, while also revealing population heterogeneity and gene–environment interactions. Concurrently, traditional Chinese medicine (TCM) has demonstrated multi-component, multi-pathway regulatory effects on uric acid production, renal and intestinal excretion, inflammatory responses, and gut microbiota. This review summarizes recent GWAS advances in hyperuricemia and compiles experimental and mechanistic studies on TCM regulation of uric acid homeostasis over the past 5 years. Furthermore, the discussion section outlines current limitations in both GWAS and TCM research, proposes potential connections between them in specific regulatory processes, and explores possible directions for future mechanistic studies and the development of intervention strategies.

Gouty arthritis (GA) is a metabolic inflammatory disorder characterized by the deposition of monosodium urate crystals. Although conventional treatments like colchicine can relieve symptoms, they come with several limitations, such as gastrointestinal side effects, hepatorenal toxicity, and poor target specificity. In contrast, natural products, known for their multi-pathway and multi-target properties, present distinct advantages and significant potential for intervening in GA. The primary pathological mechanism of GA involves the overactivation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, making its regulation a promising therapeutic approach. However, there is currently a lack of comprehensive reviews on how natural products target the NLRP3 inflammasome. Additionally, existing studies have not sufficiently classified or integrated the mechanisms involved in transcriptional and translational regulation during the priming phase, post-translational modifications, and the various pathways active during the activation phase. This article aims to address these gaps through a systematic literature review, providing an in-depth analysis of the molecular mechanisms by which natural products alleviate GA by targeting the NLRP3 inflammasome. It also critically examines the major challenges in current translational research, with the objective of offering a solid theoretical foundation and practical strategies for developing novel, effective anti-inflammatory drugs and expediting the clinical application of natural products for GA treatment.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by progressive mitochondrial dysfunction that disrupts hepatocellular metabolism, redox homeostasis, and inter-organelle communication. Hepatic metabolic zonation, maintained by spatially specialized mitochondrial networks, coordinates β-oxidation, oxidative phosphorylation, and lipid synthesis under physiological conditions. Chronic nutrient excess and insulin resistance disrupt this zonal organization, particularly in pericentral hepatocytes, leading to oxidative imbalance, defective mitochondrial quality control (MQC), and lipid accumulation. Mitochondrial injury is not confined to hepatocytes. The release of mitochondrial DNA (mtDNA), cardiolipin, and other mitochondrial danger-associated molecular patterns activates Kupffer cells and hepatic stellate cells through TLR9- and cGAS-STING-dependent pathways, thereby amplifying inflammatory and fibrogenic responses. Recent studies indicate that selected natural compounds improve mitochondrial function by enhancing AMPK-SIRT1-PGC-1α-dependent biogenesis, promoting PINK1/Parkin-mediated mitophagy, and attenuating mito-DAMP-driven innate immune activation. This review integrates liver metabolism and mitochondrial stress signaling pathways, elucidates the mechanistic framework of liver-mitochondrial interactions in MASLD, and explores pharmacological strategies targeting organelles to restore liver metabolic homeostasis.

Huayu Jiedu formula (HYJDF), a traditional Chinese herbal compound effective against acute cerebral infarction (ACI), lacks a defined mechanism of action. HYJDF's bioactive components were identified via ultra-high-performance liquid chromatography-Quadrupole-Exactive-mass spectrometry (UHPLC-QE-MS). Network pharmacology integrated the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform database-predicted ACI targets and multiple databases to construct herb-component-target networks (Cytoscape). Core targets were prioritized through protein-protein interaction network analysis (STRING) and topological filtering (degree/closeness/betweenness centrality). Pathway enrichment (Kyoto Encyclopedia of Genes and Genomes [KEGG] Database for Annotation, Visualization, and Integrated Discovery) and molecular docking (AutoDock Vina) were performed. Key findings were validated in vivo using a middle cerebral artery occlusion rat model. UHPLC-QE-MS identified 1041 components; 229 were ACI-relevant. Topological analysis revealed 29 core targets (e.g., TP53, STAT3, interleukin [IL]6, tumor necrosis factor [TNF], and Akt1). KEGG enrichment implicated the PI3K/Akt pathway. Molecular docking confirmed high-affinity binding between HYJDF components (e.g., arachidonic acid and baicalein) and targets (Akt1 and IL6). In vivo, HYJDF treatment upregulated PI3K/Akt phosphorylation, suppressed neuroinflammation, and attenuated cerebral ischemic injury. HYJDF mediates therapeutic effects against ACI primarily by activating the PI3K/Akt signaling pathway and downregulating associated inflammatory factors.

ObjectiveAsymptomatic hyperuricaemia (AH) is an independent risk factor for chronic kidney disease, cardiovascular events, and metabolic disorders. However, controversies persist regarding the clinical use of urate-lowering therapies (ULTs). This study employs a network meta-analysis (NMA) to systematically evaluate the efficacy and safety of ULTs in AH across seven key endpoints: serum uric acid (SUA), estimated glomerular filtration rate (eGFR), high-sensitivity C-reactive protein (hs-CRP), systolic blood pressure (SBP), major adverse cardiovascular events (MACE), composite renal events (CREs) and drug-induced liver injury (DILI). The findings aim to inform clinical decision-making.MethodFour databases were systematically searched from their inception to March 2025 for all relevant literature, screening and evaluating randomized controlled trials (RCTs) assessing ULTs in AH. A frequentist NMA was conducted using R software. The Risk of Bias 2.0 tool was employed for bias assessment, and therapies were ranked via P-scores. In addition, transitivity assessment, network meta-regression, and sensitivity analysis were also performed.ResultsA total of 51 studies involving 8 ULTs and 10,281 subjects were included in this NMA. Random-effects modelling showed that, compared to controls, Verinurad_Febuxostat (P-score = 0.82; pooled mean difference [95% CI]: -3.20 [-4.76 to -1.64]) was the most effective in reducing SUA, Febuxostat (P-score = 0.78; 1.91 [0.47 to 3.35]) was the most effective in improving eGFR, Topiroxostat (P-score = 0.96; -6.10 [-11.75 to -0.45]) was most effective in improving SBP, and Febuxostat (P-score = 0.78; 0.77 [0.61 to 0.98]) reduced the risk of CREs most effectively. A None of the interventions showed significant differences in hs-CRP, MACE, or DILI. The Confidence in Network Meta-Analysis (CINeMA) assessment indicated that the overall quality of evidence was low to moderate.ConclusionAvailable evidence suggests that febuxostat not only plays a significant role in lowering SUA levels but also significantly delays the decline in eGFR and reduces the risk of CREs.

Background: Gastric cancer (GC) remains a leading cause of cancer mortality. E3 ubiquitin ligases, as central regulators of protein stability and signaling within the ubiquitin–proteasome system, have been implicated in tumor progression, but their functional roles in GC are not well established. Methods: We integrated bioinformatics analysis of TCGA and GEO datasets, in vitro experiments (including cell proliferation, migration, and apoptosis assays), and computational modeling to identify key prognostic factors in GC. Results: We established two molecular subtypes (E3GC1/E3GC2) with distinct clinical outcomes and developed a 10-gene prognostic signature. The model showed moderate predictive accuracy (AUC: 0.61–0.71) and was validated externally. MMRN1 was upregulated in GC cells and its knockdown significantly inhibited malignant phenotypes. Critically, drug sensitivity analysis revealed high-risk patients were more sensitive to proteasome inhibitors (bortezomib), while low-risk patients responded better to taxane-based chemotherapy (docetaxel). Molecular docking predicted a high-confidence interaction between MMRN1 and NEDD4L, suggesting potential ubiquitination regulation. Conclusions: MMRN1 drives GC cell proliferation and migration in vitro and may be regulated by NEDD4L-mediated ubiquitination. Our study provides a foundation for E3 ligase-based patient stratification and personalized therapy selection in GC. While this study provides comprehensive multi-omics evidence supporting the role of MMRN1 in GC progression, its clinical translation is limited by the lack of in vivo validation and direct experimental evidence of NEDD4L-MMRN1 physical interaction. Further studies using animal models and clinical specimens are warranted to confirm these findings.

International guidelines recommend short-course dual antiplatelet therapy (DAPT) for secondary prevention in patients with acute minor stroke. However, the optimal duration of such therapy remains unclear. This review aims to evaluate and compare the efficacy and safety of different DAPT durations in the secondary prevention of acute minor ischemic stroke. The present study systematically searched PubMed, Embase (via Ovid), Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), and ClinicalTrials.gov to identify relevant randomized-controlled trials. The primary outcome was the incidence of all recurrent strokes. Data synthesis was performed through network meta-analysis and paired meta-analysis methodologies. A total of 7 studies with 34,646 participants were included. Compared with aspirin alone, each course of DAPT reduced the risk of recurrent stroke but increased the risk of bleeding: aspirin–clopidogrel 21 day DAPT (OR 0.75,95

ETHNOPHARMACOLOGICAL RELEVANCE:Gujin Luyan Xuming decoction (XMD), a traditional chinese medicine formula documented in the "Synopsis of the Golden Chamber", is an effective prescription for treating cerebral infarction with notable clinical efficacy. However, its molecular mechanism remains to be fully elucidated. AIM OF THE STUDY:This research seeks to clarify the molecular mechanisms by which XMD facilitates angiogenesis following cerebral infarction. METHODS:The therapeutic levels of XMD on cerebral infarction were assessed in vivo, and the bioactive constituents of XMD were identified in systemic circulation. Afterward, the RNA-seq dataset GSE137482 and single-cell sequencing dataset GSE225948 were analyzed using R software, in conjunction with WGCNA, predicted drug targets derived from bioactive components, and angiogenesis-related gene sets, to identify key drug targets. We also performed molecular docking and molecular dynamics simulation. Finally, both in vivo and in vitro experiments were conducted for validation. RESULTS:Our research showed that XMD-H yielded the most significant effect on improving ischemic brain injury. A total of 33 blood-entering components of XMD were identified using HPLC-MS/MS analysis. Network pharmacology, RNA sequencing, single-cell sequencing, and further investigations identified RAB11A as the primary target of XMD's effect in cerebral infarction. According to molecular docking and dynamics simulation, the bioactive components of XMD could partially bind with the RAB11A protein. Animal experiments demonstrated that XMD could enhance the expression of RAB11A, Wnt5a, β-catenin, VEGFA, VEGFR2, and other proteins. The outcomes of in vitro experiments indicated that XMD could further augment cell migration, lumen formation, and the expression of the aforementioned proteins. The silencing of RAB11A led to a partial reduction in XMD's efficacy in promoting cell migration, lumen formation, and the expression of proteins such as RAB11A, Wnt5a, and VEGFR2. CONCLUSIONS:XMD could affect the Wnt5a/β-catenin signaling pathway through RAB11A, thereby enhancing angiogenesis in cerebral infarction and mitigating cerebral ischemia injury.

Diabetes mellitus (DM), a metabolic disease of globally health concern, is pathologically attributed to mitochondrial dysfunction, an essential component in disease progression. Mitochondrial quality control (MQC) acts as a critical defense mechanism for metabolic homeostasis, yet its implications in DM and its complications remain incompletely understood. This study thoroughly summarizes emerging evidence that delineates the molecular processes of MQC, with an emphasis on effector protein post-translational regulation, upstream signaling hubs, and interactions with other metabolic processes including ferroptosis and lipid metabolism. We highlight newly discovered processes involving mitochondrial-derived vesicles, licensed mitophagy, and mitocytosis that broaden the regulatory landscape of MQC, going beyond the traditionally recognized process including biogenesis, dynamics and mitophagy. MQC imbalance exacerbates insulin resistance, while impaired insulin signaling reciprocally compromises mitochondrial function, creating a vicious cycle of metabolic deterioration. Despite tissue-specific pathophysiology, diabetic complications exhibit identical MQC impairment including suppressed biogenesis, fission-fusion imbalance, and deficient mitophagy. Emerging therapies including clinical hypoglycemic agents and bioactive phytochemicals demonstrate therapeutic potential by restoring MQC. However, current strategies remain anchored to classical pathways, neglecting novel MQC mechanisms such as mitocytosis. Addressing this gap demands integration of cutting-edge MQC insights into drug discovery, particularly for compounds modulating upstream regulators. Future studies must prioritize mechanistic dissection of MQC novel targets and their translational relevance in halting metabolic collapse of diabetes progression. Since mitochondrial function is a cornerstone of metabolic restoration, synergizing precision MQC modulation with multi-target interventions, holds transformative potential for refine diabetic complications therapeutics.

Non-alcoholic fatty liver disease (NAFLD), characterized by abnormal lipid accumulation in hepatocytes, is prevalent in conditions such as type 2 diabetes mellitus and obesity, which are associated with dysregulated glucose and lipid metabolism. Bile acids (BAs) are critical regulators of lipid and glucose homeostasis. Emerging research suggests that disturbances in BA metabolism not only exacerbate metabolic imbalance but also promote ferroptosis via lipid peroxidation. This review differs by systematically linking BA regulation, ferroptosis, and TCM, highlighting the multi-component and multi-target advantages of TCM in preventing and treating NAFLD. We summarize the mechanisms by which BAs regulate hepatic lipid synthesis and oxidation, and how lipid peroxidation connects to ferroptosis through glutathione/glutathione disulfide (GSH/GSSG) and reactive oxygen species (ROS). Finally, we review studies on TCM modulation of BA metabolism and ferroptosis to improve lipid peroxidation and metabolic disorders, providing timely insights into innovative therapeutic strategies for NAFLD.

BackgroundHyperuricemia (HUA), found widely in humans and birds, is a key physiological factor responsible for the development of gout. In recent years, the relationship between the gut microbiota and HUA has garnered significant attention from researchers. This study aims to explore the current research hotspots, knowledge gaps, and future research trends regarding the gut microbiota and HUA.MethodsWe performed a thorough search of the literature on gut flora and HUA published between 2005 and 2024 using the Web of Science and PubMed databases. The resulting data were analyzed using VOSviewer, CiteSpace, and Bibliometrix.ResultsIncluding 735 papers in total, the study found that the number of publications in the subject increased significantly between 2020 and 2024, with 2024 being the year with the highest number of publications. The primary research countries are highlighted as China and the United States, with institutions such as the University of California, San Diego, and Qingdao University making significant contributions. Sanjay K. Nigam and Chenyang Lu have made the most important contributions as authors. Keywords analysis highlighted high-frequency terms including “gastrointestinal microbiome,” “uric acid,” “hyperuricemia,” “inflammation,” “gout,” and “probiotics.” In the visualization map of the keyword timeline, emerging research hotspots include “diets,” “dietary fiber,” “fecal microbiota transplantation,” and “gut-kidney axis.”ConclusionThis study is the first to conduct a quantitative literature analysis in the field of gut microbiota in HUA, revealing that the core research hotspots include disease-related microbiota characteristics, probiotic therapy, microecological intervention, and the gut-distal target organ axis. The emerging hotspots focus on dietary supplementation, fecal microbiota transplantation (FMT) treatment strategies, and in-depth research on the above organ axes. Provide valuable guidance for future research directions.

BACKGROUND:Cerebral infarction significantly impairs the quality of life of affected patients, emphasizing the need for research into novel targeted therapeutic agents. For nearly 2000 years, Gujin Luyan Xuming decoction (GJLYXMD) has been a classical treatment for this condition; however, the precise molecular mechanism remains unclear. PURPOSE:This study aimed to examine the mechanism of GJLYXMD in middle cerebral artery occlusion/reperfusion (MCAO/R) rats via the integration of multi-omics approaches, network pharmacology, and molecular dynamics simulation. METHODS:The efficacy of GJLYXMD in treating cerebral ischemia-reperfusion injury (CIRI) was initially assessed in vivo. The identification of active ingredients of GJLYXMD absorbed in the brain was conducted using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Subsequently, 16S rDNA sequencing, fecal metabolomics, ischemic lateral cerebral cortex metabolomics, proteomics, and network pharmacology were employed to elucidate potential mechanisms of GJLYXMD in the treatment of CIRI. The therapeutic feasibility of GJLYXMD for CIRI was ultimately supported by molecular docking, molecular dynamics simulation, and correlation analysis. RESULTS:Pharmacodynamic assessment indicated that GJLYXMD could ameliorate cerebral ischemia injury, with the most pronounced effect observed in the GJLYXMD-H group. A total of 14 active ingredients absorbed in the brain were identified by UPLC-MS/MS analysis. Analysis of 16S rDNA and fecal metabolites indicated that GJLYXMD-H could modulate intestinal microbiota and metabolites, restore the intestinal barrier, and reduce inflammatory cytokine levels. 235 differential metabolites were identified in the cerebral cortex between the Model and GJLYXMD-H groups. The differential proteins between these groups were enriched in the P53 and necroptosis signaling pathways, further validated by network pharmacology and animal studies. Molecular docking and molecular dynamics simulation studies indicated that the primary component of GJLYXMD can bind to the P53 protein. CONCLUSION:This study identifies, for the first time, 14 active components absorbed in the brain of GJLYXMD. Besides, GJLYXMD can alter the composition of intestinal flora and fecal metabolic pathways, and inhibit P53-mediated necroptosis, consequently improving CIRI. These findings illustrate considerable translational potential of GJLYXMD in the management of CIRI and warrant further research and development.

The gut microbiota is closely associated with the onset and development of type 2 diabetes mellitus (T2DM), characterized by insulin resistance (IR) and chronic low-grade inflammation. However, despite the widespread use of first-line antidiabetic drugs, IR in diabetes and its complications continue to rise. The gut microbiota and its metabolic products may promote the development of T2DM by exacerbating IR. Therefore, regulating the gut microbiota has become a promising therapeutic strategy, with particular attention given to probiotics, prebiotics, synbiotics, and fecal microbiota transplantation. This review first examines the relationship between gut microbiota and IR in T2DM, summarizing the research progress of microbiota-based therapies in modulating IR. We then delve into how gut microbiota-related metabolic products contribute to IR. Finally, we summarize the research findings on the role of traditional Chinese medicine in regulating the gut microbiota and its metabolic products to improve IR. In conclusion, the gut microbiota and its metabolic products play a crucial role in the pathophysiological process of T2DM by modulating IR, offering new insights into potential therapeutic strategies for T2DM.

AbstractBackgroundAs the methodological quality and evidence level of the existing systematic reviews (SRs) on music as an intervention for depression have not been thoroughly evaluated, a systematic evaluation and re‐evaluation (SERE) was conducted.MethodsMultiple databases including PubMed, Web of Science, Embase, China National Knowledge Infrastructure, SinoMed, Wanfang, and the VIP database were searched for SRs and meta‐analyses (MAs) on the effectiveness of music as an intervention for depression. The literature screening, evaluation of methodological quality, and assessment of evidence level were carried out by a team of researchers. The methodological quality was evaluated using the Assessment of Multiple Systematic Reviews 2 (AMSTAR 2) scale in accordance with the 2020 Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines, and the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) criteria were utilized to assess the level of evidence.ResultsA total of 18 SRs were included in the analysis. The 2020 PRISMA guidelines were utilized to evaluate various aspects such as search terms, funding sources, statistical methods for missing values, subgroup and sensitivity analyses, certainty assessment, excluded literature citations, assessment of publication bias, protocol information, conflicts of interest, and data availability, which were rarely reported. The evaluation of the studies using the AMSTAR 2 scale revealed that one article was rated as high quality, six were rated as low quality, and 11 were rated as very low quality. Based on the GRADE criteria evaluation, the quality of the evidence was found to be inconsistent, with reports primarily consisting of medium‐quality evidence.ConclusionThe methodological quality of SRs/MAs of music as an intervention in depression is generally poor, and the level of evidence is generally low.

Gestational diabetes mellitus (GDM) is a common complication that occurs during pregnancy. Emerging evidence suggests that immune abnormalities play a pivotal role in the development of GDM. Specifically, regulatory T cells (Tregs) are considered a critical factor in controlling maternal–fetal immune tolerance. However, the specific characteristics and alterations of Tregs during the pathogenesis of GDM remain poorly elucidated. Therefore, this study aimed to investigate the changes in Tregs among pregnant women diagnosed with GDM compared to healthy pregnant women. A prospective study was conducted, enrolling 23 healthy pregnant women in the third trimester and 21 third-trimester women diagnosed with GDM. Participants were followed up until the postpartum period. The proportions of various Treg, including Tregs, mTregs, and nTregs, were detected in the peripheral blood of pregnant women from both groups. Additionally, the expression levels of PD-1, HLA-G, and HLA-DR on these Tregs were examined. The results revealed no significant differences in the proportions of Tregs, mTregs, and nTregs between the two groups during the third trimester and postpartum period. However, GDM patients exhibited significantly reduced levels of PD-1+ Tregs (P < 0.01) and HLA-G+ Tregs (P < 0.05) in the third trimester compared to healthy pregnant women in the third trimester. Furthermore, GDM patients demonstrated significantly lower levels of PD-1+ mTregs (P < 0.01) and HLA-G+ (P < 0.05) mTregs compared to healthy pregnant women in the third trimester. Overall, the proportion of Tregs did not exhibit significant changes during the third trimester in GDM patients compared to healthy pregnant women. Nevertheless, the observed dysregulation of immune regulation function in Tregs and mTregs may be associated with the development of GDM in pregnant women.