Association study of matrix metalloproteinase 3 5A/6A polymorphism with in-stent restenosis after percutaneous coronary interventions in a Han Chinese population

Du, Ji Bing; Zhang, Wei; Li, Na; Jiang, Hua; Yin, Long; Gao, Jing; Chen, Shu Tao; Cong, Hong Liang; Wei, Yi

doi:10.1177/0300060519827145

Cited by 7 publications

(6 citation statements)

References 37 publications

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“…Functional studies of the 5A/6A polymorphism have indicated that the 5A‐allele has a higher promoter activity than the 6A‐allele in both cultured fibroblasts and VSMCs in vitro (Ye et al, 1996)—a finding bolstered by gene expression studies in skin biopsies that have also found higher MMP‐3 activity in 5A‐allele carriers (Medley et al, 2003). Accordingly, it has been postulated that the 5A‐allele is associated with higher levels of circulating MMP‐3 compared to the 6A‐allele, and indeed some studies, but not all (Du et al, 2020; Gnasso et al, 2000; Samnegard et al, 2005), have found this hypothesis to hold true (El‐Aziz & Mohamed, 2016; Medley et al, 2003). Furthermore, it has been speculated that the 5A‐allele contributes to a vascular phenotype characterized by increased ECM degradation, whereas the 6A‐allele contributes to a vascular phenotype characterized by increased ECM deposition (Ye, 2006), although genetic association studies have also reported somewhat conflicting findings (Beton et al, 2016; Beyzade et al, 2003; Nojiri et al, 2003; Samnegard et al, 2005; Yamada et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Serum MMP‐3 and its association with central arterial stiffness among young adults is moderated by smoking and BMI

et al. 2021

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Central arterial stiffness is an independent predictor of cardiovascular disease. It is characterized by a marked reduction in the elastin‐collagen ratio of the arterial wall extracellular matrix (ECM), and is largely the result of degradation of various ECM components. Matrix metalloproteinase‐3 (MMP‐3) may contribute to central arterial stiffness via its involvement in ECM homeostasis and remodeling. This study examined the association between serum MMP‐3 concentrations and central arterial stiffness and potential interactions of MMP‐3 and traditional cardiovascular risk factors in a population of healthy young adults. A total of 206 participants (n = 109 females) aged 19–25 years were included in the current study. Central arterial stiffness was measured non‐invasively as carotid‐femoral pulse wave velocity (cfPWV) (m/s). MMP‐3 concentrations (ng/ml) were measured using ELISA techniques. Regression analyses were used to examine the association between cfPWV and MMP‐3, adjusting for age, sex, smoking status, body mass index (BMI), instantaneous mean arterial pressure (MAP) and heart rate, and serum C‐reactive protein. Interactions between MMP‐3 with smoking, BMI, sex, and MAP were analyzed in subsequent regression models. MMP‐3 was an independent predictor of cfPWV (β = 0.187, p = 0.007), and significant interactions between MMP‐3 and regular smoking (β = 0.291, p = 0.022), and MMP‐3 and BMI (β = 0.210, p = 0.013) were observed. Higher serum MMP‐3 concentrations were associated with a faster cfPWV and thus, greater central arterial stiffness. Interactions between MMP‐3 and smoking, and MMP‐3 and BMI may, in part, drive the association between MMP‐3 and central arterial stiffness.

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Section: Discussionmentioning

confidence: 99%

Serum MMP‐3 and its association with central arterial stiffness among young adults is moderated by smoking and BMI

et al. 2021

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“…studies on the MMP3 gene 5A/6A polymorphism (n ¼ 4519), 6 studies on the AGT gene M235T polymorphisms (n ¼ 1801), and 7 studies on the AT1R gene A1166C polymorphism (n ¼ 2477) were pooled, with characteristics managed together (Table I). Three studies (Du et al 19 on MMP-3, Ryu et al 21 on AGT, and Li et al 26 on AT1R) failed to meet the equilibrium in HWE test with P < 0.05 by the Fisher exact test. Quality assessment was based on the Newcastle-Ottawa Scale from all the included studies.…”

Section: March 2020mentioning

confidence: 99%

“…Results were generally robust in the analysis of the eNOS and MMP-3 polymorphisms under all models. For MMP3, after eliminating 1 study (Du et al 19 ), the association vanished under the heterozygote model with an OR P ¼ 0.149, under the dominant model with an OR P ¼ 0.153, and the overdominant model with an OR P ¼ 0.226. For the AGT gene, after eliminating 1 study (Volzke et al 20 ), the association vanished under the dominant model with an OR P ¼ 0.266, the heterozygote model with an OR P ¼ 0.162, and the overdominant model with an OR P ¼ 0.118.…”

Section: Sensitivity Analysismentioning

confidence: 99%

“…The subgroup analysis by ethnicity revealed that the association remained significant under the allele, dominant, and overdominant models in Asian populations with the fixed-effect model (5A vs 6A: OR ¼ 0.728; 95% CI, 0.571e0.929; P ¼ 0.011; 5A5A + 6A5A vs 6A6A: OR ¼ 0.700; 95% CI, 0.534e0.917; P ¼ 0.010; 5A5A + 6A6A vs 6A5A: OR ¼ 1.392; 95% CI, 1.057e1.832; P ¼ 0.018), with no significance observed under others models. After deletion of 1 study (Du et al 19 ), inconsistent with the HWE test, only 1 study for the Asian population was available. As for white subgroup analysis, no significant association was observed with restenosis under any models.…”

Section: March 2020mentioning

confidence: 99%

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Associations Between Polymorphisms of Endothelial Nitric Oxide Synthase, Matrix Metalloproteinase 3, Angiotensinogen, and Angiotensin II Type 1 Receptor and Risk of Restenosis After Percutaneous Coronary Intervention: A Meta-analysis

Zhou

Sang

et al. 2020

Clinical Therapeutics

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Purpose: Previous studies have reported controversial results regarding the risk of restenosis with polymorphisms of endothelial nitric oxide synthase (eNOS), matrix metalloproteinase 3 (MMP-3), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT1R) after percutaneous coronary intervention (PCI). This study aimed to summarize the association between these polymorphisms and risk of restenosis after PCI. Methods: We searched the electronic databases of PubMed, Embase, Cochrane's Library, and ClinicalTrials.gov for studies on the association of eNOS, MMP-3, AGT, and AT1R polymorphisms with restenosis. Findings: A total of 17 studies (7781 patients) were analyzed, including 5 studies on eNOS G298A (n ¼ 912), 5 studies on MMP3 5A/6A (n ¼ 4519), 6 studies on AGT M235T (n ¼ 1801), and 7 studies on AT1R A1166C (n ¼ 2477). For the G298A variant of the eNOS gene, the allele odds ratio (OR) was 1.685 (95% CI, 1.269e2.338; P < 0.001), the heterozygote OR was 2.144 (95% CI, 1.490e3.085; P < 0.001), the dominant OR was 2.078 (95% CI, 1.462e2.954; P < 0.001), and the overdominant OR was 0.496 (95% CI, 0.348e0.706; P < 0.001). For the 5A/6A variant of the MMP3 gene, the heterozygote OR was 0.839 (95% CI, 0.722e0.975; P ¼ 0.022), the dominant OR was 0.846 (95% CI, 0.733e0.976; P ¼ 0.022), and the overdominant OR was 1.141 (95% CI, 1.001e1.301; P ¼ 0.049). For the M235T variant of the AGT gene, the heterozygote OR was 1.594 (95% CI, 1.179e2.155; P ¼ 0.002), the dominant OR was 1.437 (95% CI, 1.077e1.918; P ¼ 0.014), and the overdominant OR was 0.694 (95% CI, 0.555e0.869; P ¼ 0.001). Positive results were observed in the AT1R gene A1166C polymorphism under 3 models (homozygote OR ¼ 2.009; 95% CI, 1.433e2.816; P < 0.001; recessive OR 1.874; 95% CI, 1.353e2.595; P < 0.001; and dominant OR ¼ 1.350; 95% CI, 1.105e1.649; P ¼ 0.003). Implications: The G298A variant of eNOS, the 5A/ 6A variant of MMP3, the M235T variant of AGT, and the A1166C variant of A1TR may increase the risk of restenosis after PCI.

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“…In a recent study, Du et al [52] investigated the role of 5A/6A promoter polymorphism in the matrix metalloproteinase 3 (MMP-3) gene and in-stent restenosis (ISR). An increment in the ISRs with genotype proportion of 6A6A and a decrement in the 5A allele were reported.…”

Section: Ecm Hydrogels In Cardiac Tissue Repairmentioning

confidence: 99%

Nanomaterial-based hydrogels for coronary interventions: a mini review

Saxena¹,

Pandey²

2020

Mini-invasive Surg

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Myocardial infarction (MI) has become a major health concern these days. Elevated levels of cholesterol due to improper diet cause severe damage to human health, resulting in the narrowing of blood vessels leading to MI. Different approaches have been used based on surgical and non-surgical treatments for these blockages to cure MI. In this regard, injectable and non-injectable hydrogel-based percutaneous coronary intervention has shown promising applicability for the treatment of cardiac damage and its repair. In this report, we summarize a few hydrogels based on natural polymers such as chitosan, alginate, polyethylene glycol and extracellular matrices to be used for percutaneous coronary intervention in the treatment of MI. Their structure, biological properties and biocompatibilities are discussed, and their existing challenges are also detailed. In addition, the probable solutions to overcome certain set backs are also highlighted.

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Association study of matrix metalloproteinase 3 5A/6A polymorphism with in-stent restenosis after percutaneous coronary interventions in a Han Chinese population

Cited by 7 publications

References 37 publications

Serum MMP‐3 and its association with central arterial stiffness among young adults is moderated by smoking and BMI

Serum MMP‐3 and its association with central arterial stiffness among young adults is moderated by smoking and BMI

Associations Between Polymorphisms of Endothelial Nitric Oxide Synthase, Matrix Metalloproteinase 3, Angiotensinogen, and Angiotensin II Type 1 Receptor and Risk of Restenosis After Percutaneous Coronary Intervention: A Meta-analysis

Nanomaterial-based hydrogels for coronary interventions: a mini review

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