The relation has not been reported consistently between the PON1 Q192R polymorphism and coronary heart disease (CHD). To clarify the discrepancy, we performed the present meta-analysis to evaluate the association between the PON1 gene Q192R polymorphism and CHD risk in Chinese population. We conducted a comprehensive search of the PubMed, EMBASE, and China National Knowledge Infrastructure databases for all available case–control studies. Two reviewers independently selected studies. Data were analyzed by STATA software package v 12.0. Thirteen studies investigating the association between the PON1 Q192R polymorphism and risk of CHD were selected in this meta-analysis with 4353 cases and 4882 controls. The association between the PON1 Q192R polymorphism and CHD is statistically significant under the recessive genetic model (R/R vs Q/R + Q/Q, odds ratio [OR] = 1.111, 95% confidence interval [CI] = 1.017–1.214). We observed no statistical association between PON1 Q192R polymorphism and risk of CHD under allele model (R vs Q, OR = 1.087, 95% CI = 0.976–1.209), homozygous model (RR vs QQ, OR = 1.192, 95% CI = 0.949–1.496), and dominant genetic model (Q/R + R/R vs Q/Q, OR = 1.127, 95% CI = 0.938–1.354). This meta-analysis suggests that the PON1 Q192R polymorphism has a weak association with CHD risk in Chinese.

Although observational studies have found both a positive and negative association between depression and hypercholesterolemia, the findings are mixed and contradictory. To our knowledge, this is the first study that employs the bidirectional Mendelian randomization (MR) and multivariable MR analysis with extensive genome-wide association studies (GWAS) data to examine the causal effect between depression and hypercholesterolemia. Using summary statistics obtained from GWAS of individuals with European ancestry, we utilize a bidirectional 2-sample MR approach to explore the potential causal association between hypercholesterolemia and depressive symptoms. Multivariable Mendelian randomization analysis was used to examine whether the direct causal effect of depression on the risk of hypercholesterolemia can be affected by traits associated with the increased risk of hypercholesterolemia. This MR analysis utilized inverse variance weighted (IVW), MR-Egger regression, weighted mode, and weighted median methods. Data on the summary level of depression were acquired from a GWAS that involved 500,199 participants. We used summary GWAS datasets for hypercholesterolemia including 206,067 participants. We also used another GWAS databases of hypercholesterolemiat (n = 463,010) to validate our results. By utilizing IVW, it was discovered that there is a possibility of a 31% rise in the risk of hypercholesterolemia due to depression (OR = 1.31, 95% CI = 1.10–1.57, P = .002). We found a consistent causal effect of depression on hypercholesterolemia from the IVW analyses using different hypercholesterolemia datasets. After adjustment of smoking, physical activity, and obesity, there remains significant causal relationship between depression and hypercholesterolemia (OR = 1.25, 95% CI = 1.01–1.54, P = .040). However, we did not find any evidence indicating that hypercholesterolemia leads to depression in the opposite direction. Directional pleiotropy was not observed in the MR-Egger regression analysis. Additionally, the MR-PRESSO analysis validated these discoveries. Neither the leave-one-out sensitivity test nor the funnel plots revealed any outliers. In both the unadjusted and adjusted estimates, depression has a consistent direct causal effect on hypercholesterolemia. Our study has led to an improved comprehension of the causal connections between hypercholesterolemia and depression, which could aid in the prevention and treatment of hypercholesterolemia.

Polo-like kinase 1 (PLK1) is a key regulator in mitosis and a highly potent target for anti-cancer therapies. Several PLK1 inhibitors have been developed and evaluated for cancer treatment. However, none of them has yet been approved for clinical usage, mostly due to their low response rates in cancer patients. A recent phase I trial reported a 44% partial response rate of onvansertib, a PLK1 inhibitor, in the treatment of patients with KRAS-mutated metastatic colorectal cancer, indicating that PLK1 inhibitor might be suitable for the treatment of this specific subtype of cancer. This review summarizes the results of preclinical experiments and clinical trials of PLK1 inhibitors, with colorectal cancer as a focus, in hope of facilitating future investigations in this research field.

The rising global obesity rates and related health problems have led to more studies focusing on dietary interventions. Anthocyanins have become a subject of great interest as a bioactive compound. This study employs a comprehensive bibliometric analysis of 945 publications from the Web of Science Core Collection (WoSCC) (2003-2024) to map the evolving research landscape linking anthocyanins to obesity management. Analysis using VOSviewer, CiteSpace, and R-bibliometrix revealed a substantial increase in the cumulative number of publications in the field, with the USA and China dominating in terms of research output. Keyword analysis identified current main research themes in the field: “anthocyanins”, “obesity”, “insulin resistance”, “oxidative stress” and “antioxidant activity” reflecting current mechanistic investigations into metabolic regulation and inflammatory pathways. The focus of research has shifted from initial compositional studies to molecular mechanisms and interactions, including intestinal flora regulation, metabolic and inflammatory regulation. This reveals a shift in research trends from phenomenal observations to precise interventions. Emerging frontiers emphasize interdisciplinary integration. In the future, anthocyanin and obesity research is expected to advance precision nutrition strategies as disciplines such as metabolomics and genetic engineering are integrated. Anthocyanin-rich formulations are expected to be adjunctive therapeutic agents for personalized obesity therapies. This highlights the dual role of anthocyanins as functional food ingredients and therapeutic agents. At the same time, it also maps out the critical path for future research including bioavailability optimization and the clinical validation of multi-target mechanisms. These findings provide new ideas and insights for interdisciplinary collaboration and innovation in the development of functional foods for metabolic health.

Frailty is a geriatric syndrome involving inflammation, oxidative stress, mitochondrial dysfunction, and metabolic disturbances. Metabolomics can systematically elucidate metabolic pathways and identify actionable biomarkers. This study systematically reviews the progress and evolutionary trends of metabolomics applications in frailty research from 2006 to 2025. Based on 1924 publications retrieved from the Web of Science Core Collection, systematic analyses were performed using CiteSpace, VOSviewer, SCImago Graphica, and the R package “bibliometrix”, focusing on pathway-level research hotspots and collaboration networks. The United States and China are the leading contributors. Research hotspots have shifted from macro-level biomarkers such as inflammation and protein–energy wasting to specific metabolic pathways including amino acid metabolism, energy metabolism, lipid metabolism, and tryptophan degradation. Key metabolites include sphingomyelin, butyrate, and trimethylamine-N-oxide. Emerging frontiers focus on the association between gut microbiota-derived metabolites and frailty phenotypes, as well as intervention strategies targeting these metabolites. This study provides the first systematic overview of global research progress in metabolomics and frailty, establishes a reproducible evaluation framework integrating physiology, nutrition, geriatrics, and computational biology, and identifies butyrate, trimethylamine-N-oxide, and tryptophan metabolites as potential metabolic targets for early identification and intervention.

Pulmonary arterial hypertension (PAH) is a complex and devastating disease that the underlying cellular and molecular mechanisms are largely remains unknown. This study aimed to elucidate the key hub genes and pathways in PAH by bioinformatics analysis. In the current study, we performed WGCNA analysis to systematically identify the hub genes for PAH using transcriptome microarray data. From the Gene Expression Omnibus (GEO) database, one microarray dataset (GSE113439) was downloaded for this study. There were 26 samples in this data set, including 15 PHA samples and 11 normal controls. Based on weighted correlation network analysis, 11 modules were identified and the MEgreenyellow module showed a significantly positive correlation with PAH (r = 0.93, P = 1e−06). The genes in greenyellow module were mainly significantly enriched in mitophagy related pathways by KEGG analyses. Combined with the protein–protein interaction (PPI) and co-expression networks, ten hub genes were identified as candidate biomarkers for PAH in the greenyellow module, including CTNNB1, NIPBL, ROCK2, ROCK1, SCAF11, JAK1, BIRC6, KIF5B, PPP1R12A and XRN1. These hub genes might be potential targets for clinical therapy against PAH. The molecular mechanisms involved in these genes that affected the prognosis of PAH should be further validated through biological and basic studies.