This meta-analysis was conducted to assess the association of Megsin 2093C/T, 2180C/T, C25663G gene polymorphism with the risk of IgA nephropathy (IgAN). The association literatures were identified from PubMed, Embase, Cochrane Library and CBM-disc (China Biological Medicine Database) on 1 January 2014, and eligible reports were recruited and synthesized. Seven eligible reports were recruited into this meta-analysis for the association of Megsin 2093C/T, 2180C/T, C25663G gene polymorphism with IgAN risk. In this meta-analysis, the association of Megsin 2093C/T TT genotype with IgAN risk in Asians was found. Interestingly, Megsin C25663G G allele and GG genotype were associated with the risk of IgAN in Asian population. However, Megsin 2180C/T gene polymorphism was not associated with IgAN risk in Asians. In conclusion, Megsin 2093C/T TT genotype, and C25663G G allele and GG genotype were associated with the risk of IgAN in Asian population. However, more studies should be performed in the future to confirm this association.
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http://dx.doi.org/10.3109/10799893.2014.936461 | DOI Listing |
Medicine (Baltimore)
February 2016
From the Department of Nephrology (L-TW, R-G F, JG, Q-LY, F-MD, ZW), Second Affiliated Hospital of Xi'an Jiaotong University; and Department of Oncology (MW, X-HL, Z-JD), Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Megsin is a mesangial cell-predominant gene that encodes a serpin family protein which is expressed in the renal mesangium. Overexpression of megsin has been observed in the glomeruli of patients with IgA nephropathy (IgAN). The aim of this study was to evaluate the association of megsin polymorphisms (rs1055901 and rs1055902) with IgAN in a Chinese population.
View Article and Find Full Text PDFKidney Dis (Basel)
May 2015
Renal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China.
Background: IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis worldwide. Highly variable data for disease prevalence and reports of familial clustering suggest the involvement of genetic factors in IgAN. As China is an area with a high prevalence of IgAN, Chinese scholars have made a considerable effort to reveal the underlying genetic architecture of IgAN.
View Article and Find Full Text PDFJ Recept Signal Transduct Res
April 2015
Department of Nephrology .
This meta-analysis was conducted to assess the association of Megsin 2093C/T, 2180C/T, C25663G gene polymorphism with the risk of IgA nephropathy (IgAN). The association literatures were identified from PubMed, Embase, Cochrane Library and CBM-disc (China Biological Medicine Database) on 1 January 2014, and eligible reports were recruited and synthesized. Seven eligible reports were recruited into this meta-analysis for the association of Megsin 2093C/T, 2180C/T, C25663G gene polymorphism with IgAN risk.
View Article and Find Full Text PDFRen Fail
June 2014
Department of Nephrology, Nanjing Children's Hospital, Affiliated to Nanjing Medical University, Nanjing , China and.
The association between megsin 2093C/T, 2180C/T and C25663G gene polymorphisms and IgA nephropathy (IgAN) risk remains unclear. We aimed to evaluate the association between megsin 2093C/T, 2180C/T and C25663G gene polymorphisms and IgAN risk by performing a meta-analysis. Eligible studies were searched according to predefined criteria by using electronic databases.
View Article and Find Full Text PDFCell Immunol
December 2011
Department of Nephrology, Guangdong Academy of Medical Sciences, Guangdong General Hospital, Guangzhou, PR China.
Over-expression of megsin is associated with mesangial cell (MC) proliferation and extracellular matrix (ECM) accumulation. The underlying pathogenesis is unknown. This study demonstrate that over-expression of megsin induced incorporation of [(3)H]thymidine in MCs and PDGF-BB, TGF-β1 upregulation.
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