Cited by 11Renin-Angiotensin System StudiesCoagulation, Bradykinin, Polyphosphates, and AngioedemaAcute Myocardial Infarction Research

Association of serum levels of AngII, KLK1, and ACE/KLK1 polymorphisms with acute myocardial infarction induced by coronary artery stenosis

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Dai, Shu-hong, Li, Ji-fu, Feng, Jin-bo, Li, Rui-jian, Li, Chuan-bao, Li, Zhuo, Zhang, Yun, Li, Da-qing·2016·Journal of the Renin-Angiotensin-Aldosterone System

Abstract

Introduction: The study aims to confirm the association of acute myocardial infarction (AMI) with serum angiotensin II (AngII), kallikrein1 (KLK1), and ACE/KLK1 polymorphisms. Materials and methods: Serum AngII/KLK1 levels and ACE and KLK1 genotypes were determined in 208 patients with AMI and 216 normal controls. Binary logistic regression was used for data analysis. Results: The differences in serum AngII levels were statistically significant between the groups. After adjusting for potential confounding factors, high serum levels of AngII and KLK1 significantly increased the risk of AMI. The individuals with ACE DD and KLK1 GG genotypes significantly increased the risk of AMI compared with those harboring the ACE II and KLK1 AA genotypes (OR = 8.77, 95% CI = 1.74–44.16). Conclusions: (1) Increasing the serum levels of AngII increased the risk of AMI. (2) The risk of AMI increased significantly when the serum levels of AngII and KLK1 simultaneously increased. (3) Individuals with the combined genotypes of ACE DD and KLK1 GG showed significantly increased risk of AMI compared with those with the combined genotypes of ACE II and KLK1 AA.

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  • Stimulated angiotensin II produces ROS which in turn causes mitochondrial dysfunction, mitochondrial DNA lesions, heart failure, fibrosis, and cardiac hypertrophy.

    “In addition, stimulated AngII produces ROS which in turn causes mitochondrial dysfunction, mitochondrial DNA lesions, heart failure, fibrosis, and cardiac hypertrophy (Dai et al. 2016).”

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Authors
Dai, S.-H., Li, J.-F., Feng, J.-B., Li, R.-J., Li, C.-B., Li, Z., Zhang, Y., & Li, D.-Q.
Affiliations
  • The Key Laboratory of Cardiovascular Remodelling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, China
  • Department of obstetrics and gynecology, Qilu Hospital, Shandong University, China
  • Department of emergency, Qilu Hospital, Shandong University, China
  • Shandong University (CN)
Corresponding author
Li, Da-qing
Venue
Journal of the Renin-Angiotensin-Aldosterone System
Published
2016-04
Volume
17
Issue
2
Pages
1470320316655037-1470320316655037
ISSN
  • 1470-3203 (ISSN-L)
  • 1752-8976
OpenAlex
W2471225343
Cited by
11
References
40
Citations by year
2025: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 1 · 2019: 1
FWCI
0.27
Type
journal article
Language
en
Open access
Locations
  • Journal of the Renin-Angiotensin-Aldosterone System (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Genetics › Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
Keywords
acute myocardial infarction, angiotensin II, kallikrein, ACE gene polymorphism, serum biomarkers, coronary artery stenosis, genetic susceptibility, risk factors
MeSH terms
Angiotensin II, Female, Gene Frequency, Humans, Peptidyl-Dipeptidase A, Male, Middle Aged, Myocardial Infarction, Chi-Square Distribution, Logistic Models, Case-Control Studies, Polymerase Chain Reaction, Polymorphism, Single Nucleotide, Tissue Kallikreins, Coronary Stenosis, INDEL Mutation

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