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  • Wang, Yutong  (5)
  • Zhang, Ben  (5)
  • 1
    Online Resource
    Online Resource
    Nuclear magnetic resonance-determined lipoprotein profile and risk of breast cancer: a Mendelian randomization study
    Springer Science and Business Media LLC ; 2023
    In:  Breast Cancer Research and Treatment Vol. 200, No. 1 ( 2023-07), p. 115-126
    Details
    In: Breast Cancer Research and Treatment, Springer Science and Business Media LLC, Vol. 200, No. 1 ( 2023-07), p. 115-126
    Type of Medium: Online Resource
    ISSN: 0167-6806 , 1573-7217
    URL: Article
    DOI: 10.1007/s10549-023-06930-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2004077-5
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  • 2
    Online Resource
    Online Resource
    Impact of gallstone disease on the risk of stroke and coronary artery disease: evidence from prospective observational studies and genetic analyses
    Springer Science and Business Media LLC ; 2023
    In:  BMC Medicine Vol. 21, No. 1 ( 2023-09-13)
    Details
    In: BMC Medicine, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2023-09-13)
    Abstract: Despite epidemiological evidence associating gallstone disease (GSD) with cardiovascular disease (CVD), a dilemma remains on the role of cholecystectomy in modifying the risk of CVD. We aimed to characterize the phenotypic and genetic relationships between GSD and two CVD events – stroke and coronary artery disease (CAD). Methods We first performed a meta-analysis of cohort studies to quantify an overall phenotypic association between GSD and CVD. We then investigated the genetic relationship leveraging the largest genome-wide genetic summary statistics. We finally examined the phenotypic association using the comprehensive data from UK Biobank (UKB). Results An overall significant effect of GSD on CVD was found in meta-analysis (relative risk [RR] = 1.26, 95% confidence interval [CI]  = 1.19–1.34). Genetically, a positive shared genetic basis was observed for GSD with stroke ( $${r}_{g}$$ r g =0.16, P  = 6.00 × 10 –4 ) and CAD ( $${r}_{g}$$ r g =0.27, P  = 2.27 × 10 –15 ), corroborated by local signals. The shared genetic architecture was largely explained by the multiple pleiotropic loci identified in cross-phenotype association study and the shared gene-tissue pairs detected by transcriptome-wide association study, but not a causal relationship (GSD to CVD) examined through Mendelian randomization (MR) (GSD-stroke: odds ratio [OR] = 1.00, 95%CI = 0.97–1 .03; GSD-CAD: OR = 1.01, 95%CI = 0.98–1.04). After a careful adjustment of confounders or considering lag time using UKB data, no significant phenotypic effect of GSD on CVD was detected (GSD-stroke: hazard ratio [HR] = 0.95, 95%CI = 0.83–1.09; GSD-CAD: HR = 0.98, 95%CI = 0.91–1.06), further supporting MR findings. Conclusions Our work demonstrates a phenotypic and genetic relationship between GSD and CVD, highlighting a shared biological mechanism rather than a direct causal effect. These findings may provide insight into clinical and public health applications.
    Type of Medium: Online Resource
    ISSN: 1741-7015
    URL: Article
    DOI: 10.1186/s12916-023-03072-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2131669-7
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  • 3
    Online Resource
    Online Resource
    Understanding the relationship between circulating lipids and risk of chronic kidney disease: a prospective cohort study and large-scale genetic analyses
    Springer Science and Business Media LLC ; 2023
    In:  Journal of Translational Medicine Vol. 21, No. 1 ( 2023-09-27)
    Details
    In: Journal of Translational Medicine, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2023-09-27)
    Abstract: This study aims to comprehensively investigate the phenotypic and genetic relationships between four common lipids (high-density lipoprotein cholesterol, HDL-C; low-density lipoprotein cholesterol, LDL-C; total cholesterol, TC; and triglycerides, TG), chronic kidney disease (CKD), and estimated glomerular filtration rate (eGFR). Methods We first investigated the observational association of lipids (exposures) with CKD (primary outcome) and eGFR (secondary outcome) using data from UK Biobank. We then explored the genetic relationship using summary statistics from the largest genome-wide association study of four lipids (N = 1,320,016), CKD (N case  = 41,395, N control  = 439,303), and eGFR(N = 567,460). Results There were significant phenotypic associations (HDL-C: hazard ratio (HR) = 0.76, 95%CI = 0.60–0.95; TG: HR = 1.08, 95%CI = 1.02–1.13) and global genetic correlations (HDL-C: $${r}_{g}$$ r g = − 0.132, P  = 1.00 × 10 –4 ; TG: $${r}_{g}$$ r g = 0.176; P  = 2.66 × 10 –5 ) between HDL-C, TG, and CKD risk. Partitioning the whole genome into 2353 LD-independent regions, twelve significant regions were observed for four lipids and CKD. The shared genetic basis was largely explained by 29 pleiotropic loci and 36 shared gene-tissue pairs. Mendelian randomization revealed an independent causal relationship of genetically predicted HDL-C (odds ratio = 0.91, 95%CI = 0.85–0.98), but not for LDL-C, TC, or TG, with the risk of CKD. Regarding eGFR, a similar pattern of correlation and pleiotropy was observed. Conclusions Our work demonstrates a putative causal role of HDL-C in CKD and a significant biological pleiotropy underlying lipids and CKD in populations of European ancestry. Management of low HDL-C levels could potentially benefit in reducing the long-term risk of CKD. Graphical Abstract
    Type of Medium: Online Resource
    ISSN: 1479-5876
    URL: Article
    DOI: 10.1186/s12967-023-04509-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2118570-0
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  • 4
    Online Resource
    Online Resource
    DataSheet_4.xlsx
    Frontiers Media SA ; 2023
    In:  Frontiers in Immunology Vol. 14 ( 2023-8-18)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-8-18)
    Abstract: The coronavirus disease 2019 (COVID-19) pandemic has exerted a profound influence on humans. Increasing evidence shows that immune response is crucial in influencing the risk of infection and disease severity. Observational studies suggest an association between COVID‐19 and immunoglobulin G (IgG) N-glycosylation traits, but the causal relevance of these traits in COVID-19 susceptibility and severity remains controversial. Methods We conducted a two-sample Mendelian randomization (MR) analysis to explore the causal association between 77 IgG N-glycosylation traits and COVID-19 susceptibility, hospitalization, and severity using summary-level data from genome-wide association studies (GWAS) and applying multiple methods including inverse-variance weighting (IVW), MR Egger, and weighted median. We also used Cochran’s Q statistic and leave-one-out analysis to detect heterogeneity across each single nucleotide polymorphism (SNP). Additionally, we used the MR-Egger intercept test, MR-PRESSO global test, and PhenoScanner tool to detect and remove SNPs with horizontal pleiotropy and to ensure the reliability of our results. Results We found significant causal associations between genetically predicted IgG N-glycosylation traits and COVID-19 susceptibility, hospitalization, and severity. Specifically, we observed reduced risk of COVID-19 with the genetically predicted increased IgG N-glycan trait IGP45 (OR = 0.95, 95% CI = 0.92–0.98; FDR = 0.019). IGP22 and IGP30 were associated with a higher risk of COVID-19 hospitalization and severity. Two (IGP2 and IGP77) and five (IGP10, IGP14, IGP34, IGP36, and IGP50) IgG N-glycosylation traits were causally associated with a decreased risk of COVID-19 hospitalization and severity, respectively. Sensitivity analyses did not identify any horizontal pleiotropy. Conclusions Our study provides evidence that genetically elevated IgG N-glycosylation traits may have a causal effect on diverse COVID-19 outcomes. Our findings have potential implications for developing targeted interventions to improve COVID-19 outcomes by modulating IgG N-glycosylation levels.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2023.1217444
    DOI: 10.3389/fimmu.2023.1217444.s001
    DOI: 10.3389/fimmu.2023.1217444.s002
    DOI: 10.3389/fimmu.2023.1217444.s003
    DOI: 10.3389/fimmu.2023.1217444.s004
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606827-8
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  • 5
    Online Resource
    Online Resource
    Using human genetics to understand the phenotypic association between chronotype and breast cancer
    Wiley ; 2024
    In:  Journal of Sleep Research Vol. 33, No. 3 ( 2024-05)
    Details
    In: Journal of Sleep Research, Wiley, Vol. 33, No. 3 ( 2024-05)
    Abstract: Little is known regarding the shared genetic influences underlying the observed phenotypic association between chronotype and breast cancer in women. Leveraging summary statistics from the hitherto largest genome‐wide association study conducted in each trait, we investigated the genetic correlation, pleiotropic loci, and causal relationship of chronotype with overall breast cancer, and with its subtypes defined by the status of oestrogen receptor. We identified a negative genomic correlation between chronotype and overall breast cancer ( = −0.06, p = 3.00 × 10 −4 ), consistent across oestrogen receptor‐positive ( = −0.05, p = 3.30 × 10 −3 ) and oestrogen receptor‐negative subtypes ( = −0.05, p = 1.11 × 10 −2 ). Five specific genomic regions were further identified as contributing a significant local genetic correlation. Cross‐trait meta‐analysis identified 78 loci shared between chronotype and breast cancer, of which 23 were novel. Transcriptome‐wide association study revealed 13 shared genes, targeting tissues of the nervous, cardiovascular, digestive, and exocrine/endocrine systems. Mendelian randomisation demonstrated a significantly reduced risk of overall breast cancer (odds ratio 0.89, 95% confidence interval 0.83–0.94; p = 1.30 × 10 −4 ) for genetically predicted morning chronotype. No reverse causality was found. Our work demonstrates an intrinsic link underlying chronotype and breast cancer, which may provide clues to inform management of sleep habits to improve female health.
    Type of Medium: Online Resource
    ISSN: 0962-1105 , 1365-2869
    URL: Issue
    URL: Article
    DOI: 10.1111/jsr.v33.3
    DOI: 10.1111/jsr.13973
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2007459-1
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