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Genetics and Epigenetics in the Pathology, Diagnosis and Therapeutics of Cardiovascular Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 6533

Special Issue Editors

Prof. Dr. Maria Dorobantu

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Guest Editor
1. Corresponding Member of the Romanian Academiy, 125, Calea Victoriei, Sector 1, RO-010071 Bucharest, Romania
2. Department 4-Cardiothoracic Pathology, University of Medicine and Pharmacy Carol Davila, 8, Eroii Sanitari Bvd., 050474 Bucharest, Romania
Interests: ischemic heart disease; atherosclerosis; molecular mechanisms of acute coronary syndromes; arterial hypertension; hypertensive target organ damage
Special Issues, Collections and Topics in MDPI journals
Dr. Theodora Benedek

E-Mail Website
Guest Editor
Faculty of Medicine, “George Emil Palade” University o Medicine, Pharmacy, Science and Technology of Targu Mures, 38 Gheorghe Marinescu Street, 54042 Targu Mures, Romania
Interests: vulnerable plaques; atherosclerosis; heart failure; acute coronary syndromes; interventional cardiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are the leading cause of death worldwide, being caused by complex interactions between genetic, environmental, and risk factors. While the risk factors associated with CVDs have been extensively studied, the association between genetic or epigenetic factors and CVDs is still insufficiently explored. Genetic studies have identified a significantly higher risk for CVDs in relatives of patients with premature CV death. Epigenetic factors regulate the function and expression of several genes associated with CVDs, being associated with cardiac hypertrophy, heart failure, and hypertension, or with CV risk factors such as dyslipidemia or diabetes mellitus. DNA methylation, histone modification, and noncoding RNA regulation are the most common pathways through which epigenetics influence CVD progression. This Special Issue, entitled “Genetics and Epigenetics in the Pathology, Diagnosis and Therapeutics of Cardiovascular Diseases”, aims to provide a new platform for the collection of original and review articles covering molecular studies on genetic and epigenetic factors related to CVDs. The presentation of research results reflecting the interaction between epigenetics, genetics, and CVDs at the molecular level is strongly encouraged.

Prof. Dr. Maria Dorobantu
Dr. Theodora Benedek
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cardiovascular diseases
  • epigenetics
  • DNA methylation
  • histone modifications
  • microRNAs

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Published Papers (3 papers)

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15 pages, 1718 KiB  
Article
MiRNA-21a, miRNA-145, and miRNA-221 Expression and Their Correlations with WNT Proteins in Patients with Obstructive and Non-Obstructive Coronary Artery Disease
by Alfiya Oskarovna Iusupova, Nikolay Nikolaevich Pakhtusov, Olga Alexandrovna Slepova, Yuri Nikitich Belenkov, Elena Vitalievna Privalova, Irina Vladimirovna Bure, Ekaterina Alexandrovna Vetchinkina and Marina Vyacheslavovna Nemtsova
Int. J. Mol. Sci. 2023, 24(24), 17613; https://doi.org/10.3390/ijms242417613 - 18 Dec 2023
Cited by 2 | Viewed by 1298
Abstract
MicroRNAs and the WNT signaling cascade regulate the pathogenetic mechanisms of atherosclerotic coronary artery disease (CAD) development. Objective: To evaluate the expression of microRNAs (miR-21a, miR-145, and miR-221) and the role of the WNT signaling cascade (WNT1, WNT3a, WNT4, and WNT5a) in obstructive [...] Read more.
MicroRNAs and the WNT signaling cascade regulate the pathogenetic mechanisms of atherosclerotic coronary artery disease (CAD) development. Objective: To evaluate the expression of microRNAs (miR-21a, miR-145, and miR-221) and the role of the WNT signaling cascade (WNT1, WNT3a, WNT4, and WNT5a) in obstructive CAD and ischemia with no obstructive coronary arteries (INOCA). Method: The cross-sectional observational study comprised 94 subjects. The expression of miR-21a, miR-145, miR-221 (RT-PCR) and the protein levels of WNT1, WNT3a, WNT4, WNT5a, LRP6, and SIRT1 (ELISA) were estimated in the plasma of 20 patients with INOCA (66.5 [62.8; 71.2] years; 25% men), 44 patients with obstructive CAD (64.0 [56.5; 71,0] years; 63.6% men), and 30 healthy volunteers without risk factors for cardiovascular diseases (CVD). Results: Higher levels of WNT1 (0.189 [0.184; 0.193] ng/mL vs. 0.15 [0.15–0.16] ng/mL, p < 0.001) and WNT3a (0.227 [0.181; 0.252] vs. 0.115 [0.07; 0.16] p < 0.001) were found in plasma samples from patients with obstructive CAD, whereas the INOCA group was characterized by higher concentrations of WNT4 (0.345 [0.278; 0.492] ng/mL vs. 0.203 [0.112; 0.378] ng/mL, p = 0.025) and WNT5a (0.17 [0.16; 0.17] ng/mL vs. 0.01 [0.007; 0.018] ng/mL, p < 0.001). MiR-221 expression level was higher in all CAD groups compared to the control group (p < 0.001), whereas miR-21a was more highly expressed in the control group than in the obstructive (p = 0.012) and INOCA (p = 0.003) groups. Correlation analysis revealed associations of miR-21a expression with WNT1 (r = −0.32; p = 0.028) and SIRT1 (r = 0.399; p = 0.005) protein levels in all CAD groups. A positive correlation between miR-145 expression and the WNT4 protein level was observed in patients with obstructive CAD (r = 0.436; p = 0.016). Based on multivariate regression analysis, a mathematical model was constructed that predicts the type of coronary lesion. WNT3a and LRP6 were the independent predictors of INOCA (p < 0.001 and p = 0.002, respectively). Conclusions: Activation of the canonical cascade of WNT-β-catenin prevailed in patients with obstructive CAD, whereas in the INOCA and control groups, the activity of the non-canonical pathway was higher. It can be assumed that miR-21a has a negative effect on the formation of atherosclerotic CAD. Alternatively, miR-145 could be involved in the development of coronary artery obstruction, presumably through the regulation of the WNT4 protein. A mathematical model with WNT3a and LRP6 as predictors allows for the prediction of the type of coronary artery lesion. Full article
(This article belongs to the Special Issue Genetics and Epigenetics in the Pathology, Diagnosis and Therapeutics of Cardiovascular Diseases)
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16 pages, 891 KiB  
Article
Association of CETP Gene Polymorphisms and Haplotypes with Cardiovascular Risk
by Peter Piko, Tibor Jenei, Zsigmond Kosa, Janos Sandor, Nora Kovacs, Ildiko Seres, Gyorgy Paragh and Roza Adany
Int. J. Mol. Sci. 2023, 24(12), 10281; https://doi.org/10.3390/ijms241210281 - 17 Jun 2023
Cited by 3 | Viewed by 1776
Abstract
Cholesteryl ester transfer protein (CETP) is known to influence HDL-C levels, potentially altering the profile of HDL subfractions and consequently cardiovascular risk (CVR). This study aimed to investigate the effect of five single-nucleotide polymorphisms (SNPs; rs1532624, rs5882, rs708272, rs7499892, and rs9989419) [...] Read more.
Cholesteryl ester transfer protein (CETP) is known to influence HDL-C levels, potentially altering the profile of HDL subfractions and consequently cardiovascular risk (CVR). This study aimed to investigate the effect of five single-nucleotide polymorphisms (SNPs; rs1532624, rs5882, rs708272, rs7499892, and rs9989419) and their haplotypes (H) in the CETP gene on 10-year CVR estimated by the Systematic Coronary Risk Evaluation (SCORE), the Framingham Risk Score for Coronary Heart Disease (FRSCHD) and Cardiovascular Disease (FRSCVD) algorithms. Adjusted linear and logistic regression analyses were used to investigate the association of SNPs and 10 haplotypes (H1–H10) on 368 samples from the Hungarian general and Roma populations. The T allele of rs7499892 showed a significant association with increased CVR estimated by FRS. H5, H7, and H8 showed a significant association with increased CVR based on at least one of the algorithms. The impact of H5 was due to its effect on TG and HDL-C levels, while H7 showed a significant association with FRSCHD and H8 with FRSCVD mediated by a mechanism affecting neither TG nor HDL-C levels. Our results suggest that polymorphisms in the CETP gene may have a significant effect on CVR and that this is not mediated exclusively by their effect on TG and HDL-C levels but also by presently unknown mechanisms. Full article
(This article belongs to the Special Issue Genetics and Epigenetics in the Pathology, Diagnosis and Therapeutics of Cardiovascular Diseases)
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17 pages, 2144 KiB  
Article
Tributyrin Intake Attenuates Angiotensin II-Induced Abdominal Aortic Aneurysm in LDLR-/- Mice
by Chih-Pei Lin, Po-Hsun Huang, Chi-Yu Chen, I-Shiang Tzeng, Meng-Yu Wu, Jia-Shiong Chen, Jaw-Wen Chen and Shing-Jong Lin
Int. J. Mol. Sci. 2023, 24(9), 8008; https://doi.org/10.3390/ijms24098008 - 28 Apr 2023
Viewed by 2978
Abstract
Abdominal aortic aneurysm (AAA) is a multifactorial cardiovascular disease with a high risk of death, and it occurs in the infrarenal aorta with vascular dilatation. High blood pressure acts on the aortic wall, resulting in rupture and causing life-threatening intra-abdominal hemorrhage. Vascular smooth [...] Read more.
Abdominal aortic aneurysm (AAA) is a multifactorial cardiovascular disease with a high risk of death, and it occurs in the infrarenal aorta with vascular dilatation. High blood pressure acts on the aortic wall, resulting in rupture and causing life-threatening intra-abdominal hemorrhage. Vascular smooth muscle cell (VSMC) dysregulation and extracellular matrix (ECM) degradation, especially elastin breaks, contribute to structural changes in the aortic wall. The pathogenesis of AAA includes the occurrence of oxidative stress, inflammatory cell infiltration, elastic fiber fragmentation, VSMC apoptosis, and phenotypic transformation. Tributyrin (TB) is decomposed by intestinal lipase and has a function similar to that of butyrate. Whether TB has a protective effect against AAA remains uncertain. In the present study, we established an AAA murine model by angiotensin II (AngII) induction in low-density lipoprotein receptor knockout (LDLR-/-) mice and investigated the effects of orally administered TB on the AAA size, ratio of macrophage infiltration, levels of matrix metalloproteinase (MMP) expression, and epigenetic regulation. TB attenuates AngII-induced AAA size and decreases elastin fragmentation, macrophage infiltration, and MMP expression in the medial layer of the aorta and reduces the levels of SBP (systolic blood pressure, p < 0.001) and MMP-2 (p < 0.02) in the serum. TB reduces the AngII-stimulated expression levels of MMP2 (p < 0.05), MMP9 (p < 0.05), MMP12, and MMP14 in human aortic smooth muscle cells (HASMCs). Moreover, TB and valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, suppress AngII receptor type 1 (AT1R, p < 0.05) activation and increase the expression of acetyl histone H3 by HDAC activity inhibition (p < 0.05). Our findings suggest that TB exerts its protective effect by suppressing the activation of HDAC to attenuate the AngII-induced AT1R signaling cascade. Full article
(This article belongs to the Special Issue Genetics and Epigenetics in the Pathology, Diagnosis and Therapeutics of Cardiovascular Diseases)
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