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Genetics and Genomics of Cardiovascular Diseases: Cellular Mechanisms and Therapeutic...
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Genetics and Genomics of Cardiovascular Diseases: Cellular Mechanisms and Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (20 November 2023) | Viewed by 4921

Special Issue Editor

Prof. Dr. Shu Ye

E-Mail Website
Guest Editor
Department of Cardiovascular Sciences, The University of Leicester, University Road, Leicester LE1 7RH, UK
Interests: cardiovascular; molecular medicine; genetics

Special Issue Information

Dear Colleagues,

A number of cardiovascular diseases, such as coronary artery disease, hypertension, aneurysm, and stroke, have a multifactorial aetiology with both genetic and life-style factors. Recently, population-scale genetic analyses have uncovered many genomic loci associated with these diseases. However, for most of these loci, the biological mechanism linking the genetic variants and disease risk remains unknown, hindering therapeutic translation. Functional studies of relevant genetic loci using molecular, cellular, and in vivo approaches could potentially provide a better understanding of the pathogenesis of these diseases and identify causal genes, which may point to novel therapeutic targets and facilitate drug development. This Special Issue provides a forum for research in this area, such as that on functional genomics and other omics, as well as molecular and cellular mechanistic studies, translational research, and methodology development studies. We invite the submission of original research papers as well as review articles.

Prof. Dr. Shu Ye
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • cardiovascular disease
  • coronary artery disease
  • Hypertension
  • hypertension
  • aneurysm
  • stroke
  • genetics
  • genomics
  • gene
  • single-nucleotide polymorphism
  • therapeutic targets

Published Papers (4 papers)

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Research

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14 pages, 3078 KiB  
Article
Tumor Growth Ameliorates Cardiac Dysfunction
by Lama Awwad, Rona Shofti, Tali Haas and Ami Aronheim
Cells 2023, 12(14), 1853; https://doi.org/10.3390/cells12141853 - 14 Jul 2023
Cited by 2 | Viewed by 1108
Abstract
Heart failure and cancer are the deadliest diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeling. Here, we [...] Read more.
Heart failure and cancer are the deadliest diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeling. Here, we examined cardiac remodeling following transverse aortic constriction (TAC) in the presence or absence of proliferating cancer cells. We show that tumor-bearing mice, of two different cancer cell lines, display reduced cardiac hypertrophy, lower fibrosis and improved cardiac contractile function following pressure overload induced by TAC surgery. Integrative analysis of qRT-PCR, flow cytometry and immunofluorescence identified tumor-dependent M1-to-M2 polarization in the cardiac macrophage population as a mediator of the beneficial tumor effect on the heart. Importantly, tumor-bearing mice lacking functional macrophages fail to improve cardiac function and display sustained fibrosis. Full article
(This article belongs to the Special Issue Genetics and Genomics of Cardiovascular Diseases: Cellular Mechanisms and Therapeutic Opportunities)
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12 pages, 972 KiB  
Article
C-Reactive Protein Level and the Genetic Variant rs1130864 in the CRP Gene as Prognostic Factors for 10-Year Cardiovascular Outcome
by Susanne Schulz, Selina Rehm, Axel Schlitt, Madlen Lierath, Henriette Lüdike, Britt Hofmann, Kerstin Bitter and Stefan Reichert
Cells 2023, 12(13), 1775; https://doi.org/10.3390/cells12131775 - 04 Jul 2023
Cited by 2 | Viewed by 1097
Abstract
Background: Cardiovascular disease (CVD) is the primary cause of premature death and disability worldwide. There is extensive evidence that inflammation represents an important pathogenetic mechanism in the development and prognosis of CVD. C-reactive protein (CRP) is a potential marker of vascular inflammation and [...] Read more.
Background: Cardiovascular disease (CVD) is the primary cause of premature death and disability worldwide. There is extensive evidence that inflammation represents an important pathogenetic mechanism in the development and prognosis of CVD. C-reactive protein (CRP) is a potential marker of vascular inflammation and plays a direct role in CVD by promoting vascular inflammation. The objective of this study (ClinTrials.gov identifier: NCT01045070) was to assess the prognostic impact of CRP protein levels and genetic variants of CRP gene events on cardiovascular (CV) outcome (10-year follow-up) in patients suffering from CVD. Methods: CVD patients were prospectively included in this study (n = 1002) and followed up (10 years) regarding combined CV endpoint (CV death, death from stroke, myocardial infarction (MI), and stroke/transient ischemic attack (TIA)). CRP protein level (particle-enhanced immunological turbidity test) and genetic variants (rs1130864, rs1417938, rs1800947, rs3093077; polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) after DNA extraction from EDTA-blood) were evaluated. Results: In survival analyses, increased CRP protein levels of ≥5 mg/L (log-rank test: p < 0.001, Cox regression: p = 0.002, hazard ratio = 1.49) and CT + TT genotype of rs1130864 (log-rank test: p = 0.041; Cox regression: p = 0.103, hazard ratio = 1.21) were associated with a weaker CV prognosis considering combined CV endpoint. Conclusions: Elevated CRP level and genetic variant (rs1130864) were proven to provide prognostic value for adverse outcome in CVD patients within the 10-year follow-up period. Full article
(This article belongs to the Special Issue Genetics and Genomics of Cardiovascular Diseases: Cellular Mechanisms and Therapeutic Opportunities)
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13 pages, 4389 KiB  
Article
Allele-Specific Epigenetic Regulation of FURIN Expression at a Coronary Artery Disease Susceptibility Locus
by Wei Yang, Junjun Cao, David G. McVey and Shu Ye
Cells 2023, 12(13), 1681; https://doi.org/10.3390/cells12131681 - 21 Jun 2023
Viewed by 1049
Abstract
Genome-wide association studies have revealed an association between the genetic variant rs17514846 in the FURIN gene and coronary artery disease. We investigated the mechanism through which rs17514846 modulates FURIN expression. An analysis of isogenic monocytic cell lines showed that the cells of the [...] Read more.
Genome-wide association studies have revealed an association between the genetic variant rs17514846 in the FURIN gene and coronary artery disease. We investigated the mechanism through which rs17514846 modulates FURIN expression. An analysis of isogenic monocytic cell lines showed that the cells of the rs17514846 A/A genotype expressed higher levels of FURIN than cells of the C/C genotype. Pyrosequencing showed that the cytosine (in a CpG motif) at the rs17514846 position on the C allele was methylated. Treatment with the DNA methylation inhibitor 5-aza-2′-deoxycytidine increased FURIN expression. An electrophoretic mobility super-shift assay with a probe corresponding to the DNA sequence at and around the rs17514846 position of the C allele detected DNA-protein complex bands that were altered by an anti-MeCP2 antibody. A chromatin immunoprecipitation assay with the anti-MeCP2 antibody showed an enrichment of the DNA sequence containing the rs17514846 site. siRNA-mediated knockdown of MeCP2 caused an increase in FURIN expression. Furthermore, MeCP2 knockdown increased monocyte migration and proliferation, and this effect was diminished by a FURIN inhibitor. The results of our study suggest that DNA methylation inhibits FURIN expression and that the coronary artery disease-predisposing variant rs17514846 modulates FURIN expression and monocyte migration via an allele-specific effect on DNA methylation. Full article
(This article belongs to the Special Issue Genetics and Genomics of Cardiovascular Diseases: Cellular Mechanisms and Therapeutic Opportunities)
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Review

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20 pages, 1002 KiB  
Review
The Genetics of Coronary Artery Disease: A Vascular Perspective
by Leon N. K. Quaye, Catherine E. Dalzell, Panos Deloukas and Andrew J. P. Smith
Cells 2023, 12(18), 2232; https://doi.org/10.3390/cells12182232 - 08 Sep 2023
Viewed by 1238
Abstract
Genome-wide association studies (GWAS) have identified a large number of genetic loci for coronary artery disease (CAD), with many located close to genes associated with traditional CAD risk pathways, such as lipid metabolism and inflammation. It is becoming evident with recent CAD GWAS [...] Read more.
Genome-wide association studies (GWAS) have identified a large number of genetic loci for coronary artery disease (CAD), with many located close to genes associated with traditional CAD risk pathways, such as lipid metabolism and inflammation. It is becoming evident with recent CAD GWAS meta-analyses that vascular pathways are also highly enriched and present an opportunity for novel therapeutics. This review examines GWAS-enriched vascular gene loci, the pathways involved and their potential role in CAD pathogenesis. The functionality of variants is explored from expression quantitative trait loci, massively parallel reporter assays and CRISPR-based gene-editing tools. We discuss how this research may lead to novel therapeutic tools to treat cardiovascular disorders. Full article
(This article belongs to the Special Issue Genetics and Genomics of Cardiovascular Diseases: Cellular Mechanisms and Therapeutic Opportunities)
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