Xinping Wang

Ms. Xinping Wang


Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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2 October 2017 in Lipids in Health and Disease
Verified
Journal Article
Open access
PDF file
XWXinping Wang
Xinping Wang
JHJia He
Jia He
HGHeng Guo
Heng Guo
LMLati Mu
Lati Mu
YHYun-Hua Hu
Yun-Hua Hu
SGShuxia Guo
Shuxia Guo
This study aims to investigate association between six single nucleotide polymorphisms(SNPs) in APOA1 gene and types of obesity with the risk of low level HDL-C in the pastoral area of northwest China. A total of 1267 individuals including 424 patients with low HDL-C disease and 843 health subjects were analyzed based on matched for age, sex. SNPShot technique was used to detect the genotypes of rs670, rs5069, rs5072, rs7116797, rs2070665 and rs1799837 in APOA1 gene. The relationship between above six SNPs and types of obesity with low HDL-C disease was analyzed by binary logistic regression. Carriers with rs670 G allele were more likely to get low HDL-C disease (OR = 1.46, OR95%CI: 1.118–1.915; P = 0.005); The genotypic and allelic frequencies of rs5069, rs5072, rs7116797, rs2070665, rs1799837 revealed no significant differences between cases and controls (P < 0.05); with reference to normal weight, Waist circumference (WC), Waist-to-hip ratio (WHR) individuals, respectively, general obesity measured by BMI had 2.686 times (OR95%CI: 1.695–4.256; P < 0.01), abdominal obesity measured by WC had 1.925 times (OR95%CI: 1.273–2.910; P = 0.002) and abdominal obesity measured by WHR had 1.640 times (OR95%CI: 1.114–2.416; P = 0.012) risk to get low HDL-C disease; APOA1 rs670 interacted with obesity (no matter general obesity or abdominal obesity) on low HDL-C disease. APOA1 gene may be associated with low HDL-C disease in the pastoral area of northwest China; obesity was the risk factor for low HDL-C disease; the low HDL-C disease is influenced by APOA1, obesity, and their interactions.

28 July 2020 in Lipids in Health and Disease
Verified
Journal Article
Open access
PDF file
XWXinping Wang
Xinping Wang
SGShuxia Guo
Shuxia Guo
YHYunhua Hu
Yunhua Hu
HGHeng Guo
Heng Guo
XZXianghui Zhang
Xianghui Zhang
RMRulin Ma
Rulin Ma
Background: Low high-density lipoprotein cholesterol (HDL-C) disease with unknown etiology has a high prevalence in the Xinjiang Kazak population. In this study, long noncoding RNAs (lncRNAs) that might play a role in low HDL-C disease were identified. Methods: Plasma samples from 10 eligible individuals with low HDL disease and 10 individuals with normal HDL-C levels were collected. The lncRNA profiles for 20 Xinjiang Kazak individuals were measured using microarray analysis. Results: Differentially expressed lncRNAs and mRNAs with fold-change values not less than 1.5 and FDR-adjusted P-values less than 0.05 were screened. Bioinformatic analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and network analyses, were used to determine relevant signaling pathways and predict potential target genes. In total, 381 lncRNAs and 370 mRNAs were differentially expressed based on microarray analysis. Compared with those in healthy individuals, several lncRNAs were upregulated or downregulated in patients with low HDL-C disease, among which TCONS_00006679 was most significantly upregulated and TCONS_00011823 was most significantly downregulated. GO and KEGG pathway analyses as well as co-expression networks of lncRNAs and mRNAs revealed that the platelet activation pathway and cardiovascular disease were associated with low HDL-C disease. Conclusions: Potential target genes integrin beta-3 (ITGB3) and thromboxane A2 receptor (TBXA2R) were regulated by the lncRNAs AP001033.3–201 and AC068234.2–202, respectively. Both genes were associated with cardiovascular disease and were involved in the platelet activation pathway. AP001033.3–201 and AC068234.2–202 were associated with low HDL-C disease and could play a role in platelet activation in cardiovascular disease. These results reveal the potential etiology of dyslipidemia in the Xinjiang Kazakh population and lay the foundation for further validation using large sample sizes.