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Biology
Special Issues
Genetic and Genomic Insights into Cardiovascular Disease
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Genetic and Genomic Insights into Cardiovascular Disease

A Special Issue of Biology (ISSN 2079-7737) belonging to the section "Genetics and Genomics".

Deadline for manuscript submissions: 15 May 2027 | Viewed by 894

Editors

Prof. Dr. Silvio Zaina

E-Mail Website
Guest Editor
Department of Medical Sciences, Division of Health Sciences, Leon Campus, University of Guanajuato, Leon 37320, Mexico
Interests: atherosclerosis; epigenetics; epigenomics; cardiovascular therapy; mouse models
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Carol C. Shoulders

E-Mail Website1 Website2
Guest Editor
Department of Endocrinology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London Charterhouse Square, London EC1M 6BQ, UK
Interests: lipids; cardiovascular risk factors; genomics and genetics; DNA and RNA therapies; intracellular transport and pseudokinases

Special Issue Information

Dear Colleagues,

This Special Issue is designed to publish a series of articles that advance our mechanistic understanding of the role of genetic variants and epigenetic modifications that contribute to cardiovascular disease (CVD) pathogenesis. The reason for this is three-fold: first, the wealth of genetic data that has emerged from genome-wide association studies that have identified variants associated with the development of CVD risk factors, and the development of in vitro and in vivo models to determine their functionality at the individual cell level, in specific genetic settings, and in a temporal and spatial manner; second, the increasing availability of large-scale single-cell epigenomic data and RNA sequencing datasets for analysing gene expression profiles in multiple cell populations that populate healthy and atherosclerotic vascular tissue; third, the significant advancements in computational methodologies to evaluate the cellular connections between CVD risk phenotypes, atheroma, CVD progression and regression. In this Special Issue, original research articles and reviews are welcome.

Prof. Dr. Silvio Zaina
Prof. Dr. Carol C. Shoulders
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology 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

  • coronary and carotid atheroma
  • lipids
  • thrombosis
  • inflammation
  • vascular calcification
  • vascular smooth muscle cells
  • foam cells
  • endothelium
  • immune cells
  • epigenetics
  • genetic variation
  • gene expression and proteomics
  • cell and disease models

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Published Papers (1 paper)

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Research

15 pages, 1932 KB  
Article
Premature Coronary Artery Disease, Association with Relative Blood Number of Mitochondrial DNA Copies in Mexican Population—Results of GEA Study
by Rosalinda Posadas-Sánchez, Marco Sánchez-Guerra, Citlalli Osorio-Yáñez, Giovanny Fuentevilla-Alvarez, Guillermo Cardoso-Saldaña, José Manuel Fragoso and Gilberto Vargas-Alarcón
Biology 2026, 15(18), 1572; https://doi.org/10.3390/biology15181572 - 8 Sep 2026
Viewed by 268
Abstract
The mitochondrial DNA copy number (mtDNA-CN) is considered an indirect indicator of the number of mitochondria and of mitochondrial dysfunction; its decrease may indirectly reflect mitochondrial DNA (mtDNA) alterations. A reduction in mtDNA-CN is associated with the development of cardiovascular diseases, including coronary [...] Read more.
The mitochondrial DNA copy number (mtDNA-CN) is considered an indirect indicator of the number of mitochondria and of mitochondrial dysfunction; its decrease may indirectly reflect mitochondrial DNA (mtDNA) alterations. A reduction in mtDNA-CN is associated with the development of cardiovascular diseases, including coronary artery disease (CAD). The study evaluates the association of relative blood mtDNA-CN with premature CAD (pCAD) and cardiometabolic factors among Mexican individuals from the GEA (Genetics of Atherosclerotic Disease) Mexican cohort. Relative blood mtDNA-CN was quantified by real-time PCR in 835 patients with pCAD and 896 control subjects (defined as a coronary artery calcium score of zero, assessed by computed tomography). Associations were evaluated using logistic regression (odds ratio [95% confidence interval]) adjusted for potential confounders. Compared with controls, patients with pCAD exhibited significantly lower relative blood mtDNA-CN (5.6 [3.5–9.8] vs. 9.1 [5.1–13.2]. p < 0.001). Similar results were observed in the sex-stratified analysis. Specifically, relative blood mtDNA-CN in women (6.2 [3.8–9.9]) and men (5.5 [3.4–9.7]) with pCAD was lower than that in women (9.5 [6.3–13.7]) and men (8.2 [5.5–12.5]) from the control group (p < 0.001). After adjusting for age, sex, body mass index, smoking status, LDL-cholesterol, type 2 diabetes mellitus, hypertension and physical activity, higher relative blood mtDNA-CN showed a negative association with pCAD (0.903 [0.881–0.927], p = 4.96 × 10−15). This association remained significant in men (0.894 [0.866–0.922], p = 2.90 × 10−12) and women (0.917 [0.876–0.960], p = 2.1 × 10−4). Among patients with pCAD, an inverse correlation was observed between relative blood mtDNA-CN and total abdominal fat (p = 0.001), visceral fat (p = 0.015), and subcutaneous fat (p = 0.004). Overall, our results show that reduced relative blood mtDNA-CN is associated with pCAD, which could be indicative of mitochondrial alterations. Furthermore, the inverse correlation between relative blood mtDNA-CN and total, visceral, and subcutaneous abdominal fat suggests a link between mitochondrial dysfunction and abdominal adiposity in patients with pCAD. These findings support that decreased relative blood mtDNA-CN may serve as a marker associated with the presence of pCAD and for adipose tissue alterations in Mexican women and men. Full article
(This article belongs to the Special Issue Genetic and Genomic Insights into Cardiovascular Disease)
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