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Pharmacogenomics of Cardiovascular Disease
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Pharmacogenomics of Cardiovascular Disease

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (20 October 2023) | Viewed by 6975

Special Issue Editor

Prof. Dr. Shanqun Jiang

E-Mail Website
Guest Editor
School of Life Sciences, Anhui University, Hefei, China
Interests: pharmacogenetics/-genomics; epigenetics; biostatistics and bioinformatics; pharmacoepidemiology; cardiovascular disease prevention and therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We would like to invite you to participate in this Special Issue, “Pharmacogenomics of Cardiovascular Disease: The Road to Precision Medicine”.

Cardiovascular disease (CVD) is the leading cause of death worldwide, accounting for ~32% of all global deaths. The contributions of genetic variants, traditional risk factors (e.g., hyperlipidemia, hypertension) and health behavior (e.g., smoking, nutrition) and their comorbidities to mortality are not entirely understood. In clinical practice, considerable interindividual variability in response to cardiovascular pharmacotherapy such as statins, ACEIs, and β-blockers exists, from being efficacious to inducing severe adverse events. Broad clinical and genetic heterogeneity in CVD risk and therapeutic efficacy highlights the urgent need for precision phenotyping. Precision medicine integrates clinical and health record datasets with advanced panomics (i.e., genomics, transcriptomics, epigenomics, metabolomics, and microbiomics) to uncover vascular disease phenotypes and select corresponding pharmacotherapeutics based on the analytical results within the framework of interactome networks. Personalized medicine offers the potential to optimize the risk–reward profile of cardiovascular drugs by tailoring diagnostic and treatment strategies according to the individual patient with CVD.

The purpose of this Special Issue is to host research and review papers on the modification of genetic variability in response to cardiovascular drugs and their potential molecular mechanisms. New results, confirmatory results, and contradictory results will also be considered for publication.

Prof. Dr. Shanqun Jiang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiovasular diseases (hyperlipidemia/hypertension/atherosclerosis/strokes)
  • pharmacogenetics/-genomics
  • epigenetics
  • precision medicine
  • statins
  • ACEIs
  • other cardiovascular agents

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

16 pages, 910 KiB  
Article
Lipid-Associated GWAS Loci Predict Antiatherogenic Effects of Rosuvastatin in Patients with Coronary Artery Disease
by Stanislav Kononov, Iuliia Azarova, Elena Klyosova, Marina Bykanova, Mikhail Churnosov, Maria Solodilova and Alexey Polonikov
Genes 2023, 14(6), 1259; https://doi.org/10.3390/genes14061259 - 13 Jun 2023
Cited by 2 | Viewed by 1823
Abstract
We have shown that lipid-associated loci discovered by genome-wide association studies (GWAS) have pleiotropic effects on lipid metabolism, carotid intima-media thickness (CIMT), and CAD risk. Here, we investigated the impact of lipid-associated GWAS loci on the efficacy of rosuvastatin therapy in terms of [...] Read more.
We have shown that lipid-associated loci discovered by genome-wide association studies (GWAS) have pleiotropic effects on lipid metabolism, carotid intima-media thickness (CIMT), and CAD risk. Here, we investigated the impact of lipid-associated GWAS loci on the efficacy of rosuvastatin therapy in terms of changes in plasma lipid levels and CIMT. The study comprised 116 CAD patients with hypercholesterolemia. CIMT, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) were measured at baseline and after 6 and 12 months of follow-up, respectively. Genotyping of fifteen lipid-associated GWAS loci was performed by the MassArray-4 System. Linear regression analysis adjusted for sex, age, body mass index, and rosuvastatin dose was used to estimate the phenotypic effects of polymorphisms, and p-values were calculated through adaptive permutation tests by the PLINK software, v1.9. Over one-year rosuvastatin therapy, a decrease in CIMT was linked to rs1689800, rs4846914, rs12328675, rs55730499, rs9987289, rs11220463, rs16942887, and rs881844 polymorphisms (Pperm < 0.05). TC change was associated with rs55730499, rs11220463, and rs6065906; LDL-C change was linked to the rs55730499, rs1689800, and rs16942887 polymorphisms; and TG change was linked to polymorphisms rs838880 and rs1883025 (Pperm < 0.05). In conclusion, polymorphisms rs1689800, rs55730499, rs11220463, and rs16942887 were found to be predictive markers for multiple antiatherogenic effects of rosuvastatin in CAD patients. Full article
(This article belongs to the Special Issue Pharmacogenomics of Cardiovascular Disease)
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9 pages, 568 KiB  
Article
The Influence of Structural Variants of the CES1 Gene on the Pharmacokinetics of Enalapril, Presumably Due to Linkage Disequilibrium with the Intronic rs2244613
by Anna Ikonnikova, Ruslan Kazakov, Tatiana Rodina, Artem Dmitriev, Evgeniy Melnikov, Alexander Zasedatelev and Tatiana Nasedkina
Genes 2022, 13(12), 2225; https://doi.org/10.3390/genes13122225 - 27 Nov 2022
Cited by 3 | Viewed by 2114
Abstract
Variants in the CES1 gene encoding carboxylesterase 1 may affect the metabolism of enalapril to the active metabolite enalaprilat. It was shown that the A allele of rs71647871 and the C allele of rs2244613 led to a decrease in plasma enalaprilat concentrations. This [...] Read more.
Variants in the CES1 gene encoding carboxylesterase 1 may affect the metabolism of enalapril to the active metabolite enalaprilat. It was shown that the A allele of rs71647871 and the C allele of rs2244613 led to a decrease in plasma enalaprilat concentrations. This study aimed to estimate the effect of structural haplotypes of CES1 containing the pseudogene CES1P1, or a hybrid of the gene and the pseudogene CES1A2, on the pharmacokinetics of enalapril. We included 286 Caucasian patients with arterial hypertension treated with enalapril. Genotyping was performed using real-time PCR and long-range PCR. Peak and trough plasma enalaprilat concentrations were lower in carriers of CES1A2. The studied haplotypes were in linkage disequilibrium with rs2244613: generally, the A allele was in the haplotype containing the CES1P1, and the C allele was in the haplotype with the CES1A2. Thus, carriers of CES1A2 have reduced CES1 activity against enalapril. Linkage disequilibrium of the haplotype containing the CES1P1 or CES1A2 with rs2244613 should be taken into account when genotyping the CES1 gene. Full article
(This article belongs to the Special Issue Pharmacogenomics of Cardiovascular Disease)
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12 pages, 972 KiB  
Article
Genetic Polymorphisms Associated with Prothrombin Time and Activated Partial Thromboplastin Time in Chinese Healthy Population
by Fan Zhang, Guangyan Mu, Zhiyan Liu, Qiufen Xie, Hanxu Zhang, Shuang Zhou, Zhe Wang, Kun Hu, Zining Wang, Xia Zhao, Yimin Cui and Qian Xiang
Genes 2022, 13(10), 1867; https://doi.org/10.3390/genes13101867 - 15 Oct 2022
Cited by 1 | Viewed by 2522
Abstract
(1) Background: The purpose of this study was to evaluate the effect of gene polymorphisms on prothrombin time (PT) and activated partial thromboplastin time (APTT) in a healthy Chinese population. (2) Methods: A total of 403 healthy volunteers from a series of novel [...] Read more.
(1) Background: The purpose of this study was to evaluate the effect of gene polymorphisms on prothrombin time (PT) and activated partial thromboplastin time (APTT) in a healthy Chinese population. (2) Methods: A total of 403 healthy volunteers from a series of novel oral anticoagulants (NOACs) bioequivalence trials in China were included. Coagulation tests for PT and APTT were performed in the central lab at Peking University First Hospital. Whole-exome sequencing (WES) and genome-wide association analysis were performed. (3) Results: In the correlation analysis of PT, 105 SNPs from 84 genes reached the genome-wide significance threshold (p < 1 × 10−5). Zinc Finger Protein 594 (ZNF594) rs184838268 (p = 4.50 × 10−19) was most significantly related to PT, and Actinin Alpha 1 (ACTN1) was found to interact most with other candidate genes. Significant associations with previously reported candidate genes Aurora Kinase B (AURKB), Complement C5(C5), Clock Circadian Regulator (CLOCK), and Histone Deacetylase 9(HDAC9) were detected in our dataset (p < 1 × 10−5). PiggyBac Transposable Element Derived 2(PGBD2) rs75935520 (p = 4.49 × 10−6), Bromodomain Adjacent To Zinc Finger Domain 2A(BAZ2A) rs199970765 (p = 5.69 × 10−6) and Protogenin (PRTG) rs80064850 (p = 8.69 × 10−6) were significantly correlated with APTT (p < 1 × 10−5). The heritability values of PT and APTT were 0.83 and 0.64, respectively; (4) Conclusion: The PT and APTT of healthy populations are affected by genetic polymorphisms. ZNF594 and ACTN1 variants could be novel genetic markers of PT, while PRTG polymorphisms might be associated with APTT levels. The findings could be attributed to ethnic differences, and need further investigation. Full article
(This article belongs to the Special Issue Pharmacogenomics of Cardiovascular Disease)
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