Role of proteinase-activated receptor-1 gene polymorphisms in susceptibility to chronic obstructive pulmonary disease

Cm, Yun; Xy, Sang

doi:10.4238/2015.october.26.18

Cited by 8 publications

(7 citation statements)

References 21 publications

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“…Previous family and twin studies have shown the role of genetic factors in COPD susceptibility [9]. Recently, some authors have used genetic polymorphisms to explain the genetic contribution to the development of COPD, and several candidate genes such as proteinase-activated receptor-1 [10], plasminogen activator inhibitor-1 [11], and β 2-adrenergic receptor [12] were reported to have an association with COPD susceptibility.…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphism of Angiotensin-Converting Enzyme and Chronic Obstructive Pulmonary Disease Risk: An Updated Meta-Analysis

Kang

Kim

Chung

et al. 2016

BioMed Research International

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The relationship between polymorphism of the angiotensin I converting enzyme (ACE) gene and chronic obstructive pulmonary disease (COPD) has been examined in many previous studies. However, their results were controversial. Therefore, we performed a meta-analysis to evaluate the relationship between the ACE gene and the risk of COPD. Fourteen case-control studies were included in this meta-analysis. The pooled p value, odds ratio (OR), and 95% confidence interval (95% CI) were used to investigate the strength of the association. The meta-analysis was performed using comprehensive meta-analysis software. Our meta-analysis results revealed that ACE polymorphisms were not related to the risk of COPD (p > 0.05 in each model). In further analyses based on ethnicity, we observed an association between insertion/deletion polymorphism of the ACE gene and risk of COPD in the Asian population (codominant 2, OR = 3.126, 95% CI = 1.919–5.093, p < 0.001; recessive, OR = 3.326, 95% CI = 2.190–5.050, p < 0.001) but not in the Caucasian population (p > 0.05 in each model). In conclusion, the present meta-analysis indicated that the insertion/deletion polymorphism of the ACE gene may be associated with susceptibility to COPD in the Asian population but not in the Caucasian population. However, the results of the present meta-analysis need to be confirmed in a larger sample.

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Section: Introductionmentioning

confidence: 99%

Genetic Polymorphism of Angiotensin-Converting Enzyme and Chronic Obstructive Pulmonary Disease Risk: An Updated Meta-Analysis

Kang

Kim

Chung

et al. 2016

BioMed Research International

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“…The relationship between the polymorphism of the gene encoding ACE and COPD has been addressed in numerous prior studies; however, these studies have yielded ambivalent results [43][44][45] . Prior studies have demonstrated the role of genetic factors in susceptibility to COPD; in part, susceptibility to COPD was found to be associated with polymorphism of proteinase-activated receptor-1 46 , plasminogen activator inhibitor-1 47 and β2-adrenergic receptors 48 . A study of relationship between COPD and ACE activity has shown the activity of ACE to depend on oxygen concentrations in the blood; therefore, increases in ACE levels due to COPD-associated hypoxia may cause severe tissue damage 49 .…”

Section: Discussionmentioning

confidence: 99%

The role of insertion-deletion polymorphism of the ACE gene in development of arterial hypertension in patients with chronic obstructive pulmonary disease

Maksiv

Krynytska

Koval

2020

Bangladesh J Med Sci

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Objective. This study aims to establish the role of insertion-deletion polymorphism of the angiotensin-converting enzyme gene in development of arterial hypertension in patients with chronic obstructive pulmonary disease. Materials and Methods: The study group consisted of 96 patients: Group 1 (25 individuals with COPD), Group 2 (23 individuals with AH), Group 3 (28 individuals with COPD and AH). The control group consisted of the 20 healthy subjects. I/D genotypes of ACE were determined by polymerase chain reaction (PCR) amplification. Plasma ACE activity was determined photometrically by a commercially available kit. Results and Discussion: The distribution of polymorphic variants of the ACE gene among COPD-only patients genotype spreading was close to the data obtained in controls. In hypertensive patients, there were fewer ID heterozygotes and more ІІ homozygotes compared to controls. In the COPD+AH category of patients, II genotype was predominant in 7.1% subjects, DD genotype was predominant in 10.0% subjects and the proportion of ID heterozygotes was 17.1% lower compared to controls. The II genotype had a positive relationship with patient age and a negative relationship with body weights and respiratory rates of COPD+AH patients. The ID genotype was associated with increased respiratory rates; however, its correlation with the duration of the disease was negative. Conclusion: The data obtained in the study allow suggesting that polymorphism of the ACE gene doesn’t relate to development of AH in patients with COPD. The highest activity of ACE was found in patients with combination of COPD and AH; maximum findings of ACE activity were seen in patients with DD genotype. Bangladesh Journal of Medical Science Vol.19(3) 2020 p.543-551

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“…Activated PARs mediate a number of pathophysiologic pathways involved in inflammatory and fibrotic diseases of different organs throughout the body, including the brain, lung, heart, liver, kidney, and gastrointestinal tract. For example, PAR-1 gene polymorphisms are associated with liver fibrosis [58], chronic obstructive pulmonary disease [59], and sarcoidosis [60], whereas PAR-1 expression is elevated during acute and chronic human liver injury [61]. Similarly, PAR-2 activation leads to increased TGF-b production and induces a profibrogenic phenotype in human hepatic stellate cells [62].…”

Section: Targeting Pars In Fibrotic Diseasesmentioning

confidence: 99%

Targeting coagulation factor receptors – protease‐activated receptors in idiopathic pulmonary fibrosis

Lin

Borensztajn

Spek

2017

Journal of Thrombosis and Haemostasis

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Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease with a 5-year mortality rate of > 50% and unknown etiology. Treatment options remain limited and, currently, only two drugs are available, i.e. nintedanib and pirfenidone. However, both of these antifibrotic agents only slow down the progression of the disease, and do not remarkably prolong the survival of IPF patients. Hence, the discovery of new therapeutic targets for IPF is crucial. Studies exploring the mechanisms that are involved in IPF have identified several possible targets for therapeutic interventions. Among these, blood coagulation factor receptors, i.e. protease-activated receptors (PARs), are key candidates, as these receptors mediate the cellular effects of coagulation factors and play central roles in influencing inflammatory and fibrotic responses. In this review, we will focus on the controversial role of the coagulation cascade in the pathogenesis of IPF. In the light of novel data, we will attempt to reconciliate the apparently conflicting data and discuss the possibility of pharmacologic targeting of PARs for the treatment of fibroproliferative diseases.

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Role of proteinase-activated receptor-1 gene polymorphisms in susceptibility to chronic obstructive pulmonary disease

Cited by 8 publications

References 21 publications

Genetic Polymorphism of Angiotensin-Converting Enzyme and Chronic Obstructive Pulmonary Disease Risk: An Updated Meta-Analysis

Genetic Polymorphism of Angiotensin-Converting Enzyme and Chronic Obstructive Pulmonary Disease Risk: An Updated Meta-Analysis

The role of insertion-deletion polymorphism of the ACE gene in development of arterial hypertension in patients with chronic obstructive pulmonary disease

Targeting coagulation factor receptors – protease‐activated receptors in idiopathic pulmonary fibrosis

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