Association of factor XIII Val34Leu polymorphism and coronary artery disease: A meta-analysis

Jung, Junhee; Song, Gwan Gyu; Kim, Jae Hoon; Seo, Young Ho; Choi, Sung Jae

doi:10.5603/cj.a2016.0070

Cited by 14 publications

(11 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Coronary artery disease (CAD), as the most common etiology of heart attack and death in the world, is a multifactorial disease caused by the combined impact of genes [1]. The main etiology of CAD is characterized by defective endothelial function; however, the underlying mechanism has not been fully elucidated despite the high incidence of CAD [2].…”

Section: Introductionmentioning

confidence: 99%

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Zhang¹,

He²,

Shi³

2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: This study aimed to analyze the impact of microRNA-499 (miR-499) on the inflammatory damage of endothelial cells during coronary artery disease (CAD) via the targeting of PDCD4 through the NF-kB/ TNF-α signaling pathway. Methods: A total of 216 CAD patients (CAD group) and 90 healthy people (normal group) were enrolled in our study. Endothelial cells were collected and assigned into normal, OX-LDL, negative control (NC), miR-499 inhibitor, miR-499 mimic, PDCD4 siRNA, and miR-499 inhibitor + PDCD4 siRNA groups. The qRT-PCR and western blotting were performed to detect the mRNA and protein expression levels of PDCD4 and miR-499. The MTT assay was performed to determine cell viability, ELISA was performed to determine the expression levels of inflammatory factors, and flow cytometry assay to evaluate cell apoptosis. Results: Increased miR-499 expression and decreased PDCD4 expression in the plasma were observed in the CAD group compared with the normal group, demonstrating a negative correlation between miR-499 and PDCD4. Compared to the normal and miR-499 inhibitor groups, the survival rate of cells and PDCD4 expression were decreased; and the expressions of miR-499, IL-6, IL-8, IL-1β, TNF-α, NF-kB, VCAM-1, ICAM-1 and MCP-1 and the apoptosis rate were all elevated in the OX-LDL, NC, miR-499 mimic, PDCD4 siRNA and miR-499 inhibitor + PDCD4 siRNA groups. Compared to the OX-LDL, NC and miR-499 inhibitor + PDCD4 siRNA groups, PDCD4 expression and the survival rate of cells were increased; and the IL-6, IL-8, IL-1β, TNF-α, NF-κB, VCAM-1, ICAM-1 and MCP-1 expression levels and the apoptosis rate were all reduced in the miR-499 inhibitor group. In the PDCD4 siRNA group, PDCD4 expression and the survival rate of cells were lower, and the expression levels of IL-6, IL-8, IL-1β, TNF-α, NF-κB, VCAM-1, ICAM-1 and MCP-1 and the apoptosis rate were all higher compared with the miR-499 mimic group. In the miR-499 inhibitor + PDCD4 siRNA group, PDCD4 expression and the survival rate of cells were higher, and the expression levels of IL-6, IL-8, IL-1β, TNF-α, NF-κB, VCAM-1, ICAM-1, and MCP-1 and the apoptosis rate were all lower than those in the PDCD4 siRNA group. Conclusion: Down-regulated miR-499 expression increased PDCD4 expression and protected endothelial cells from inflammatory damage during CAD by inhibiting the NF-κB/TNF-α signaling pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Zhang¹,

He²,

Shi³

2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Although the modified fibrin phenotype seems to be related to premature CAD, there was no association between the F13A1 Val34Leu genetic variant and MI in young patients in other studies [22, 23]. Nevertheless, the most recently published meta-analysis revealed that F13A1 Val34Leu variant was associated with CAD risk, especially MI, without differences in age [24].…”

Section: Discussionmentioning

confidence: 99%

Increased coagulation factor XIII activity but not genetic variants of coagulation factors is associated with myocardial infarction in young patients

Ambroziak

Kuryłowicz

Budaj

2019

J Thromb Thrombolysis

View full text Add to dashboard Cite

The aim of the study was to investigate the possible role of coagulation factor XIII (FXIII) plasma activity and its gene (F13A1) Val34Leu variant as well as thrombospondin-2 gene (THBS2) T/G 3′UTR and thrombospondin-4 gene (THBS4) Ala387Pro variants in the development of myocardial infarction (MI) in young patients. The studied group consisted of 158 patients aged < 50 years with MI, and the control groups consisted of 150 healthy people aged < 50 years and 202 patients suffering from MI aged ≥ 50 years. Factor XIII activity was measured by photometric assay; genetic variants were determined using the restriction fragment length polymorphism (RFLP) method. FXIII activity was significantly higher in the young MI group compared with young healthy controls and the MI ≥ 50 group (126.2 U/dl vs. 109.6 U/dl, p < 0.0001; 126.2 U/dl vs. 119.8 U/dl, p = 0.01, respectively). FXIII activity did not correlate with F13A1 gene variants. F13A1, THBS2 and THBS4 genotypes were equally distributed in all studied groups. There was also no statistically significant differences in the prevalence of the extended CC/TT/GG haplotype of F13A1/THBS2/THBS4 variants between the young MI group and the young healthy control group and between the young MI group and the MI aged ≥ 50 group. In conclusion, our study revealed that increased FXIII activity is associated with an increased risk of MI in young patients. None of studied single genetic variants—F13A1 Val34Leu, THBS2 T/G 3′UTR and THBS4 Ala387Pro—and the extended CC/TT/GG haplotype of F13A1/THBS2/THBS4 genes was associated with MI in young age.

show abstract

“…Genetic determinants of fibrin clot properties have naturally been sought as a means of risk stratification and to identify possible treatment targets. Focus points have been the FXIII Val34Leu and PAI-1 4G/4G polymorphisms which have both been linked to CAD risk in large meta-analyses [15,16]. However, the association between these genetic variants and CAD is modest in size and is dependent on other factors, mainly fibrinogen, and the potential mechanisms through which these polymorphisms may influence fibrin clot structure are also not clear [17].…”

Section: Fibrin Clot Propertiesmentioning

confidence: 99%

Fibrin clot properties in coronary artery disease: new determinants and prognostic markers

Larsen¹,

Hvas²

2021

Polish Archives of Internal Medicine

View full text Add to dashboard Cite

Despite improved diagnosis and treatment options, coronary artery disease (CAD) is still a leading cause of mortality and morbidity worldwide. Established risk factors as smoking, hypercholesterolemia, and hypertension only partly explain the pathophysiology of CAD.Besides the well-known role of platelets in atherosclerosis and arterial thrombus formation, reduced endogenous fibrinolytic activity may play a key role for CAD formation and progression. Thus, biomarkers of fibrinolysis may be future CAD risk markers. In this review we provide an overview of regulators of fibrinolysis and the main factors of importance to fibrin clot formation including coagulation factor XIII, thrombin and fibrinogen. We summarize markers of altered fibrinolysis and current laboratory methods applied in clinical practice and research. We present today's evidence on fibrin clot properties in patients with stable CAD or acute coronary syndrome compared to healthy individuals and the significance of altered fibrinolysis as a risk for coronary thrombotic disease. In conclusion, we find evidence that altered fibrin clot properties and impaired fibrinolysis appears to contribute significantly to the thromboembolic risk in CAD patients. Therefore, more research is crucial in order to clarify whether modulation of the fibrinolytic system may pave the way for improved treatment of CAD.

show abstract

Association of factor XIII Val34Leu polymorphism and coronary artery disease: A meta-analysis

Abstract: (Cardiol J 2017; 24, 1: 74-84)

Cited by 14 publications

References 19 publications

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Increased coagulation factor XIII activity but not genetic variants of coagulation factors is associated with myocardial infarction in young patients

Fibrin clot properties in coronary artery disease: new determinants and prognostic markers

Contact Info

Product

Resources

About