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Biology
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Environmental Chemicals and Cardiovascular Disease: Models and Mechanism
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Environmental Chemicals and Cardiovascular Disease: Models and Mechanism

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 10673

Special Issue Editors

Dr. Zunwei Chen

E-Mail Website
Guest Editor
The Harvard T.H. Chan School of Public Health, Harvard University, Boston, MA 02115, USA
Interests: environmental toxicology; high throughput in vitro screening; mixtures; reactive oxygen species; risk assessment
Dr. Jingshu Chen

E-Mail Website
Guest Editor
Harvard Medical School, Harvard University, Boston, MA 02115, USA
Interests: long non-coding RNA; nuclear receptor; bioinformatics; animal science
Dr. Lauren Lewis

E-Mail Website
Guest Editor
Takeda Pharmaceuticals, Tokyo 183-8509, Japan
Interests: toxicology; miRNA; epigenetics; transcriptomics

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD) are a leading cause of death globally. Accumulating toxicological and epidemiologic evidence indicates exposure to environmental chemicals such as heavy metals, air pollution, and pesticides is associated with an increased risk of CVD incidence and mortality. At present, there is a critical gap in screening methods to detect potential cardiovascular toxicants, including environmental chemicals. Traditional in vivo studies can be limiting in terms of species translation as well as cost. With the advancement of technology, including 3D in vitro models, human-derived iPSCs, transcriptomics, and high content screening, there is an opportunity to improve predictive tools to de-risk chemicals and their possible cardiotoxic effects. Utilizing these up-and-coming in vitro models for toxicant screening may offer insight to mechanistic actions of environments chemicals. This is key because uncovering underlying mechanisms in response to environment chemical exposure will help to provide preventative strategies for CVD. Furthermore, by understanding how these toxicants result in disease pathogenesis, new treatment approaches for humans exposed to such chemicals can evolve.

This Special Issue aims to summarize cutting-edge research in cardiovascular models which may be used for elucidating mechanisms, therefore providing a better understanding of how environmental toxicants play a role in the development of CVD. Herein, we will highlight the most recent developments in the many different sectors of CVD research, encompassing innovative in vitro models, new computational approaches, and high throughput screening technologies. For this Special Issue, we encourage the submission of manuscripts on any aspect of CVD, and we will accept timely reviews and short- and full-length research papers which cover the aforementioned subjects

Dr. Zunwei Chen
Dr. Jingshu Chen
Dr. Lauren Lewis
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. Biology 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 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

  • environmental chemicals
  • environmental mixtures
  • cardiovascular
  • biomarkers
  • iPSCs
  • 3D culture systems
  • organ-on-a-chip
  • high throughput screening
  • transcriptomics
  • epigenetics
  • in silico modeling
  • computational approach

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Published Papers (2 papers)

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13 pages, 842 KiB  
Article
Long-Term Exposure to Ozone and Fine Particulate Matter and Risk of Premature Coronary Artery Disease: Results from Genetics of Atherosclerotic Disease Mexican Study
by Rosalinda Posadas-Sánchez, Gilberto Vargas-Alarcón, Andres Cardenas, José Luis Texcalac-Sangrador, Citlalli Osorio-Yáñez and Marco Sanchez-Guerra
Biology 2022, 11(8), 1122; https://doi.org/10.3390/biology11081122 - 27 Jul 2022
Cited by 6 | Viewed by 2286
Abstract
(1) Background: Epidemiological studies have identified associations between fine particulate matter (PM2.5) and ozone exposure with cardiovascular disease; however, studies linking ambient air pollution and premature coronary artery disease (pCAD) in Latin America are non-existing. (2) Methods: Our study was a [...] Read more.
(1) Background: Epidemiological studies have identified associations between fine particulate matter (PM2.5) and ozone exposure with cardiovascular disease; however, studies linking ambient air pollution and premature coronary artery disease (pCAD) in Latin America are non-existing. (2) Methods: Our study was a case–control analysis nested in the Genetics of Atherosclerotic Disease (GEA) Mexican study. We included 1615 participants (869 controls and 746 patients with pCAD), recruited at the Instituto Nacional de Cardiología Ignacio Chávez from June 2008 to January 2013. We defined pCAD as history of myocardial infarction, angioplasty, revascularization surgery or coronary stenosis > 50% diagnosed before age 55 in men and age 65 in women. Controls were healthy individuals without personal or family history of pCAD and with coronary artery calcification equal to zero. Hourly measurements of ozone and PM2.5 from the Atmospheric Monitoring System in Mexico City (SIMAT in Spanish; Sistema de Monitero Atmosférico de la Ciudad de México) were used to calculate annual exposure to ozone and PM2.5 in the study participants. (3) Results: Each ppb increase in ozone at 1-year, 2-year, 3-year and 5-year averages was significantly associated with increased odds (OR = 1.10; 95% CI: 1.03–1.18; OR = 1.17; 95% CI: 1.05–1.30; OR = 1.18; 95% CI: 1.05–1.33, and OR = 1.13; 95% CI: 1.04–1.23, respectively) of pCAD. We observed higher risk of pCAD for each 5 µg/m3 increase only for the 5-year average of PM2.5 exposure (OR = 2.75; 95% CI: 1.47–5.16), compared to controls. (4) Conclusions: Ozone exposure at different time points and PM2.5 exposure at 5 years were associated with increased odds of pCAD. Our results highlight the importance of reducing long-term exposure to ambient air pollution levels to reduce the burden of cardiovascular disease in Mexico City and other metropolitan areas. Full article
(This article belongs to the Special Issue Environmental Chemicals and Cardiovascular Disease: Models and Mechanism)
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26 pages, 4728 KiB  
Article
High-Throughput Chemical Screening and Structure-Based Models to Predict hERG Inhibition
by Shagun Krishna, Alexandre Borrel, Ruili Huang, Jinghua Zhao, Menghang Xia and Nicole Kleinstreuer
Biology 2022, 11(2), 209; https://doi.org/10.3390/biology11020209 - 28 Jan 2022
Cited by 12 | Viewed by 7577
Abstract
Chemical inhibition of the human ether-a -go-go-related gene (hERG) potassium channel leads to a prolonged QT interval that can contribute to severe cardiotoxicity. The adverse effects of hERG inhibition are one of the principal causes of drug attrition in clinical and pre-clinical development. [...] Read more.
Chemical inhibition of the human ether-a -go-go-related gene (hERG) potassium channel leads to a prolonged QT interval that can contribute to severe cardiotoxicity. The adverse effects of hERG inhibition are one of the principal causes of drug attrition in clinical and pre-clinical development. Preliminary studies have demonstrated that a wide range of environmental chemicals and toxicants may also inhibit the hERG channel and contribute to the pathophysiology of cardiovascular (CV) diseases. As part of the US federal Tox21 program, the National Center for Advancing Translational Science (NCATS) applied a quantitative high throughput screening (qHTS) approach to screen the Tox21 library of 10,000 compounds (~7871 unique chemicals) at 14 concentrations in triplicate to identify chemicals perturbing hERG activity in the U2OS cell line thallium flux assay platform. The qHTS cell-based thallium influx assay provided a robust and reliable dataset to evaluate the ability of thousands of drugs and environmental chemicals to inhibit hERG channel protein, and the use of chemical structure-based clustering and chemotype enrichment analysis facilitated the identification of molecular features that are likely responsible for the observed hERG activity. We employed several machine-learning approaches to develop QSAR prediction models for the assessment of hERG liabilities for drug-like and environmental chemicals. The training set was compiled by integrating hERG bioactivity data from the ChEMBL database with the Tox21 qHTS thallium flux assay data. The best results were obtained with the random forest method (~92.6% balanced accuracy). The data and scripts used to generate hERG prediction models are provided in an open-access format as key in vitro and in silico tools that can be applied in a translational toxicology pipeline for drug development and environmental chemical screening. Full article
(This article belongs to the Special Issue Environmental Chemicals and Cardiovascular Disease: Models and Mechanism)
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