Correlation between GDF-15 gene polymorphism and the formation of collateral circulation in acute ST-elevation myocardial infarction

Chen, Xiaoping; Xiao-Sen, Shang; Wang, Yanbin; Fu, Zhi-hua; Gao, Yu; Feng, Tao

doi:10.1590/1806-9282.63.12.1049

Cited by 3 publications

(4 citation statements)

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“…(SNPs)] are suggested to affect GDF15 expression; for example, rs888663 and rs1054564 located upstream of the GDF15 gene [58][59][60] are associated with CVDs. [61][62][63] Contradictory, no effect of SNPs increasing GDF15 transcription activity 62 in CVDs is also present. 60,64 In addition, SNPs in the miRNAs (miR) regulating GDF15 expression are suggested to be important as well; an example is miRSNP rs1054564 in the 3′ UTR of the GDF15 transcript, which causes allele-specific translational repression via has-miR-1233-3p.…”

Section: Regulation Of Growth Differentiation Factor 15 On the Genetimentioning

confidence: 99%

“…Growth differentiation factor 15 is located on chromosome 19p12‐13.1, with a length of 2.746 base pairs containing two exons separated by an intron 15,57 ( Figure ). Various gene polymorphisms [single nucleotide polymorphisms (SNPs)] are suggested to affect GDF15 expression; for example, rs888663 and rs1054564 located upstream of the GDF15 gene 58–60 are associated with CVDs 61–63 . Contradictory, no effect of SNPs increasing GDF15 transcription activity 62 in CVDs is also present 60,64 .…”

Section: Growth Differentiation Factor 15mentioning

confidence: 99%

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Growth differentiation factor 15 in adverse cardiac remodelling: from biomarker to causal player

2020

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Heart failure is a growing health issue as a negative consequence of improved survival upon myocardial infarction, unhealthy lifestyle, and the ageing of our population. The large and complex pathology underlying heart failure makes diagnosis and especially treatment very difficult. There is an urgent demand for discriminative biomarkers to aid disease management of heart failure. Studying cellular pathways and pathophysiological mechanisms contributing to disease initiation and progression is crucial for understanding the disease process and will aid to identification of novel biomarkers and potential therapeutic targets. Growth differentiation factor 15 (GDF15) is a proven valuable biomarker for different pathologies, including cancer, type 2 diabetes, and cardiovascular diseases. Although the prognostic value of GDF15 in heart failure is robust, the biological function of GDF15 in adverse cardiac remodelling is not fully understood. GDF15 is a distant member of the transforming growth factor-β family and involved in various biological processes including inflammation, cell cycle, and apoptosis. However, more research is suggesting a role in fibrosis, hypertrophy, and endothelial dysfunction. As GDF15 is a pleiotropic protein, elucidating the exact role of GDF15 in complex disease processes has proven to be a challenge. In this review, we provide an overview of the role GDF15 plays in various intracellular and extracellular processes underlying heart failure, and we touch upon crucial points that need consideration before GDF15 can be integrated as a biomarker in standard care or when considering GDF15 for therapeutic intervention.

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Section: Regulation Of Growth Differentiation Factor 15 On the Genetimentioning

confidence: 99%

Section: Growth Differentiation Factor 15mentioning

confidence: 99%

Growth differentiation factor 15 in adverse cardiac remodelling: from biomarker to causal player

2020

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“…Hitherto, dozens of single nucleotide polymorphism (SNP) loci have been found, among which rs1059519 and 1059369, in the exon region, are under intensive focus. However, current studies on these two loci are mainly focused on cardiovascular disease[ 19 , 20 ] and malignant tumor[ 21 ], while correlation with the infection of hepatitis virus has not yet been reported. Thus, the present study aimed to explore the correlation between MIC-1 and the chronic infection of HCV by determining the expression level of MIC-1 and the gene polymorphism in the exon region in CHC patients and healthy subjects who cleared the screening examination.…”

Section: Introductionmentioning

confidence: 99%

Associations of content and gene polymorphism of macrophage inhibitory factor-1 and chronic hepatitis C virus infection

Yang

Wang

Yao

et al. 2020

WJG

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BACKGROUND The expression of macrophage inhibitory factor-1 (MIC-1) is increased in peripheral blood of patients with chronic hepatitis and liver cirrhosis. However, whether MIC-1 gene polymorphism is correlated with relevant diseases is not yet reported. AIM To explore the correlation between gene polymorphism in MIC-1 exon region and chronic hepatitis C virus (HCV) infection. METHODS This case-control study enrolled 178 patients with chronic hepatitis C (CHC) in the case group, and 82 healthy subjects from the same region who had passed the screening examination comprised the control group. The genotypes of rs1059369 and rs1059519 loci in the MIC-1 gene exon were detected by DNA sequencing. Also, the MIC-1 level, liver function metrics, liver fibrosis metrics, and HCV RNA load were determined. Univariate analysis was used to compare the differences and correlations between the two groups with respect to these parameters. Multivariate logistic regression was used to analyze the independent relevant factors of CHC. RESULTS The plasma MIC-1 level in the CHC group was higher than that in the control group ( P < 0.05), and it was significantly positively correlated with alanine aminotransferase, aspartate aminotransferase (AST), type III procollagen N-terminal peptide (known as PIIINP), type IV collagen, and HCV RNA ( P < 0.05), whereas negatively correlated with total protein and albumin ( P < 0.05). The genotype and allele frequency distribution at the rs1059519 locus differed between the two groups ( P < 0.05). The allele frequency maintained significant difference after Bonferroni correction ( Pc < 0.05). Logistic multiple regression showed that AST, PIIINP, MIC-1, and genotype GG at the rs1059519 locus were independent relevant factors of CHC ( P < 0.05). Linkage disequilibrium (LD) was found between rs1059369 and rs1059519 loci, and significant difference was detected in the distribution of haplotype A-C between the CHC and control groups ( P < 0.05). Meanwhile, we found the MIC-1 level trend to increase among rs1059519 genotypes ( P = 0.006) and the level of MIC-1 in GG genotype to be significantly higher than CC genotype ( P = 0.009, after Bonferroni correction). CONCLUSION Plasma MIC-1 level was increased in CHC patients and correlated with liver cell damage, liver fibrosis metrics, and viral load. The polymorphism at the MIC-1 gene rs1059519 locus was correlated with HCV infection, and associated with the plasma MIC-1 level. G allele and GG genotype may be an important susceptible factor for CHC.

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“…There are many SNPs in the human MIC-1 gene, and most of them are nonsense SNPs, while SNPs in exons may cause changes in the amino acid sequence of the MIC-1 precursor protein. Among them, rsl059519 and 1059369 are the most focused sites, several studies have found that the polymorphisms of MIC-1 are crucial genetic factors on cardiovascular diseases [ 21 , 22 ] and malignant tumors [ 23 ]. However, There are no report about influence of MIC-1 gene polymorphism in hepatitis b virus so far.…”

Section: Introductionmentioning

confidence: 99%

Association of macrophage inhibitory factor -1 polymorphisms with antiviral efficacy of type 1b chronic hepatitis C

Chen

Lou

et al. 2021

Mol Cell Biochem

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The expression of macrophage inhibitory factor-1 (MIC-1) increases in patients with chronic hepatitis C (CHC), but whether MIC-1 level and its polymorphism affect the antiviral efficacy of CHC has not yet been reported. The present study aimed to investigate the association between MIC-1 polymorphism and antiviral efficacy in patients with CHC genotype 1b (CHC 1b). A total of 171 patients with CHC1b were recruited. The polymorphisms of rs1059369 and rs1059519 in MIC-1 were detected by DNA sequencing. All patients received a standard dose of polyethylene glycol interferon + ribavirin (PR regimen), and divided into response, nonresponse, sustained virological response (SVR), and non-sustained virological response (NSVR) groups based on HCV RNA levels. The genotype distribution of the two single nucleotide polymorphisms (SNPs) did not differ between the response and nonresponse groups, SVR and non-SVR groups. However, the level of MIC-1 was positively correlated with ALT, AST, PIIINP, CIV, and HCV RNA (P < 0.05). Compared to before treatment, the level of MIC-1 in plasma was significantly decrease in the response group but not in the non-responsive group. Our results suggest that the level of MIC-1 in CHC1b is correlated with liver cell injury, liver fibrosis index, and viral load. However, the polymorphism of rs1059369 and rs1059519 may have negligible impact in expression of MIC-1 and efficacy of antiviral therapy in CHC patient.

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Correlation between GDF-15 gene polymorphism and the formation of collateral circulation in acute ST-elevation myocardial infarction

Abstract: There was correlation between GDF-15-3148C/G polymorphism and the formation of collateral circulation in patients with acute STEMI.

Cited by 3 publications

References 13 publications

Growth differentiation factor 15 in adverse cardiac remodelling: from biomarker to causal player

Growth differentiation factor 15 in adverse cardiac remodelling: from biomarker to causal player

Associations of content and gene polymorphism of macrophage inhibitory factor-1 and chronic hepatitis C virus infection

Association of macrophage inhibitory factor -1 polymorphisms with antiviral efficacy of type 1b chronic hepatitis C

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