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Your search keyword '"Hexiang Peng"' showing total 3 results
Start Over Author "Hexiang Peng" Topic genetics
3 results on '"Hexiang Peng"'

1. Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases

Author

Siyue Wang, Hexiang Peng, Feng Chen, Chunfang Liu, Qiwen Zheng, Mengying Wang, Jiating Wang, Huan Yu, Enci Xue, Xi Chen, Xueheng Wang, Meng Fan, Xueying Qin, Yiqun Wu, Jin Li, Ying Ye, Dafang Chen, Yonghua Hu, and Tao Wu

Subjects
Medicine, Genetics, QH426-470
Abstract

Abstract Background Comorbidities of coronavirus disease 2019 (COVID-19)/coronary heart disease (CHD) pose great threats to disease outcomes, yet little is known about their shared pathology. The study aimed to examine whether comorbidities of COVID-19/CHD involved shared genetic pathology, as well as to clarify the shared genetic variants predisposing risks common to COVID-19 severity and CHD risks. Methods By leveraging publicly available summary statistics, we assessed the genetically determined causality between COVID-19 and CHD with bidirectional Mendelian randomization. To further quantify the causality contributed by shared genetic variants, we interrogated their genetic correlation with the linkage disequilibrium score regression method. Bayesian colocalization analysis coupled with conditional/conjunctional false discovery rate analysis was applied to decipher the shared causal single nucleotide polymorphisms (SNPs). Findings Briefly, we observed that the incident CHD risks post COVID-19 infection were partially determined by shared genetic variants. The shared genetic variants contributed to the causality at a proportion of 0.18 (95% CI 0.18–0.19) to 0.23 (95% CI 0.23–0.24). The SNP (rs10490770) located near LZTFL1 suggested direct causality (SNPs → COVID-19 → CHD), and SNPs in ABO (rs579459, rs495828), ILRUN(rs2744961), and CACFD1(rs4962153, rs3094379) may simultaneously influence COVID-19 severity and CHD risks. Interpretation Five SNPs located near LZTFL1 (rs10490770), ABO (rs579459, rs495828), ILRUN (rs2744961), and CACFD1 (rs4962153, rs3094379) may simultaneously influence their risks. The current study suggested that there may be shared mechanisms predisposing to both COVID-19 severity and CHD risks. Genetic predisposition to COVID-19 is a causal risk factor for CHD, supporting that reducing the COVID-19 infection risk or alleviating COVID-19 severity among those with specific genotypes might reduce their subsequent CHD adverse outcomes. Meanwhile, the shared genetic variants identified may be of clinical implications for identifying the target population who are more vulnerable to adverse CHD outcomes post COVID-19 and may also advance treatments of ‘Long COVID-19.’

Published
2023
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2. Blood DNA methylation markers associated with type 2 diabetes, fasting glucose, and HbA1c levels: An epigenome-wide association study in 316 adult twin pairs

Author

Liming Cong, Canqing Yu, Hua Wang, Yu Liu, Dianjianyi Sun, Hexiang Peng, Yuanjie Pang, Zengchang Pang, Biqi Wang, Chunxiao Liao, Zhaonian Wang, Xianping Wu, Tao Huang, Liming Li, Wenjing Gao, Jun Lv, and Weihua Cao

Subjects
Adult, medicine.medical_specialty, Type 2 diabetes, Biology, Epigenesis, Genetic, Fasting glucose, Epigenome, Hba1c level, Internal medicine, Genetics, medicine, Humans, Epigenomics, Glycated Hemoglobin, Fasting, DNA Methylation, medicine.disease, Glucose, Endocrinology, Diabetes Mellitus, Type 2, CpG site, DNA methylation, CpG Islands, TXNIP, Genome-Wide Association Study
Abstract

DNA methylation plays an important role in the development and etiology of type 2 diabetes; however, few epigenomic studies have been conducted on twins. Herein, a two-stage study was performed to explore the associations between DNA methylation and type 2 diabetes, fasting plasma glucose, and HbA1c. DNA methylation in 316 twin pairs from the Chinese National Twin Registry (CNTR) was measured using Illumina Infinium BeadChips. In the discovery sample, the results revealed that 63 CpG sites and 6 CpG sites were significantly associated with fasting plasma glucose and HbA1c, respectively. In the replication sample, cg19690313 in TXNIP was associated with both fasting plasma glucose (P = 1.23 × 10-17, FDR < 0.001) and HbA1c (P = 2.29 × 10-18, FDR < 0.001). Furthermore, cg04816311, cg08309687, and cg09249494 may provide new insight in the metabolic mechanism of HbA1c. Our study provides solid evidence that cg19690313 on TXNIP correlates with HbA1c and fasting plasma glucose levels.

Published
2021

3. GLA variation p.E66Q identified as the genetic etiology of Fabry disease using exome sequencing

Author

Sanchuan Luo, Xiaojuan Xu, Xuehong Zhang, Yu Zheng, Jia-Da Li, Kun Xia, Hongliang Yao, Hui Guo, Lusi Zhang, Hao Peng, Zhengmao Hu, and Hexiang Peng

Subjects
Adult, Male, 0301 basic medicine, Adolescent, medicine.disease_cause, 03 medical and health sciences, symbols.namesake, Asian People, Genetics, medicine, Humans, Exome, Family, Allele, Alleles, Exome sequencing, Sanger sequencing, Kidney, Mutation, Alpha-galactosidase, biology, High-Throughput Nucleotide Sequencing, General Medicine, Middle Aged, medicine.disease, Fabry disease, Pedigree, 030104 developmental biology, medicine.anatomical_structure, alpha-Galactosidase, symbols, biology.protein, Fabry Disease, Female
Abstract

Fabry disease (FD) was an X-linked lysosomal storage disorder resulting from a deficiency in glycosphingolipid catabolism caused by mutations in the α-galactosidase A gene GLA. Variant FD patients did not present with classical symptoms during childhood and were undiagnosed or misdiagnosed with other kidney diseases, such as chronic glomerulonephritis (CGN). In this study, we utilized exome sequencing and Sanger sequencing identified the variation p.E66Q of GLA completely co-segregated with the disease phenotype in a Chinese family, which previously been diagnosed as possible CGN. Female patients exhibited preferential X-chromosome inactivation (XCI) of the normal p.E66 allele, as indicated by XCI analysis. By measuring α-Gal A activity, we found that male patients in the pedigree had just little enzymatic activity while female patients had residual enzymatic activity. These patients were diagnosed with renal variant FD in subsequent clinical review. Our results directly implicated the GLA mutation p.E66Q as the genetic etiology of the Chinese renal variant FD pedigree.

Published
2016

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