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JCDD
Special Issues
Cellular Mechanisms of Cardiac Damage and Healing
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Cellular Mechanisms of Cardiac Damage and Healing

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Cardiac Development and Regeneration".

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 8274

Special Issue Editors

Dr. Ronald Vagnozzi

E-Mail Website
Guest Editor
Department of Medicine, Division of Cardiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
Interests: innate immunity; fibrosis; wound healing; cell crosstalk; kinase signaling
Dr. Pearl Quijada

E-Mail Website
Guest Editor
Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095, USA
Interests: cardiac development; epicardium; epithelial-to-mesenchymal transition; angiogenesis; paracrine signaling; cardiac repair and regeneration

Special Issue Information

Dear Colleagues,

We are pleased to announce a Special Issue of the Journal of Cardiovascular Development and Disease on the “Cellular Mechanisms of Cardiac Damage and Healing”. The heart is exquisitely sensitive to tissue insults such as hypoxia, mechanical or neurohormonal stress, or chronic inflammation. This, coupled with emerging data on the complex and heterogeneous makeup of cardiac cell types, has presented a unique challenge—to elucidate how the heart adapts (or fails to adapt) to various tissue stresses at the individual cell level and through intracellular signaling cues.

This Special Issue of the JCDD will focus on (1) molecular mechanisms of cardiac cell death during tissue injury (including programmed necrosis, apoptosis, ER stress and proteostasis, and mitochondrial/metabolic impairment) and (2) cellular and tissue-level responses to these injury events (signaling to innate and adaptive immune cells through DAMPs and lipid-based resolution mediators, fibroblast activation and extracellular matrix production, vascular remodeling, and chemokine/cytokine signaling across the epicardium, myocardium, and endothelium). The editors seek original research articles, full-length or short form reviews, and descriptions of technical/methodological advances which are based on tissue injury models of adult cardiac disease, developmental or congenital heart diseases, or systems of cardiac regeneration such as zebrafish or neonatal mammals. We also encourage potential contributors to reach out to us in advance to discuss their submission and how it may fit within this Special Issue.

Dr. Ronald Vagnozzi
Dr. Pearl Quijada
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. Journal of Cardiovascular Development and Disease 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

  • cell death
  • cytokines
  • inflammation
  • ischemia
  • fibrosis
  • paracrine
  • regeneration
  • vasculature

Published Papers (4 papers)

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Research

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15 pages, 4329 KiB  
Article
P66Shc (Shc1) Zebrafish Mutant Line as a Platform for Testing Decreased Reactive Oxygen Species in Pathology
by Landon Haslem, Jennifer M. Hays, Xin A. Zhang and Franklin A. Hays
J. Cardiovasc. Dev. Dis. 2022, 9(11), 385; https://doi.org/10.3390/jcdd9110385 - 9 Nov 2022
Viewed by 1667
Abstract
Reactive oxygen species (ROS) dysregulation exacerbates many pathologies but must remain within normal ranges to maintain cell function. Since ROS-mediated pathology and routine cell function are coupled, in vivo models evaluating low-ROS background effects on pathology are limited. Some models alter enzymatic antioxidant [...] Read more.
Reactive oxygen species (ROS) dysregulation exacerbates many pathologies but must remain within normal ranges to maintain cell function. Since ROS-mediated pathology and routine cell function are coupled, in vivo models evaluating low-ROS background effects on pathology are limited. Some models alter enzymatic antioxidant expression/activity, while others involve small molecule antioxidant administration. These models cause non-specific ROS neutralization, decreasing both beneficial and detrimental ROS. This is detrimental in cardiovascular pathology, despite the negative effects excessive ROS has on these pathologies. Thus, current trends in ROS-mediated pathology have shifted toward selective inhibition of ROS producers that are dysregulated during pathological insults, such as p66Shc. In this study, we evaluated a zebrafish heterozygote p66Shc hypomorphic mutant line as a low-ROS myocardial infarction (MI) pathology model that mimics mammalian MI. Our findings suggest this zebrafish line does not have an associated negative phenotype, but has decreased body mass and tissue ROS levels that confer protection against ROS-mediated pathology. Therefore, this line may provide a low-ROS background leading to new insights into disease. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiac Damage and Healing)
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13 pages, 1684 KiB  
Article
The CCR2+ Monocyte Subsets Increase in Obese Boys but Not Girls with Abnormally High Carotid Intima-Media Thickness: A Pilot Study
by María José Garcés-Hernández, Karen Pedraza-Escudero, Nayely Garibay-Nieto, Joselin Hernández-Ruiz, Jessica Lakshmi Prieto-Chávez, Lourdes Andrea Arriaga-Pizano, Eréndira Villanueva-Ortega, Galileo Escobedo, Aaron Noe Manjarrez-Reyna, Juan Carlos López-Alvarenga, José Luis Pérez-Hernández and Gloria Queipo-García
J. Cardiovasc. Dev. Dis. 2022, 9(10), 330; https://doi.org/10.3390/jcdd9100330 - 29 Sep 2022
Cited by 2 | Viewed by 1874
Abstract
The differential contribution of monocyte subsets expressing the C-C chemokine receptor 2 (CCR2) to subclinical atherosclerosis in girls and boys is unclear. In this pilot study, we compared classical, intermediate, and nonclassical monocyte subsets expressing CCR2 in 33 obese children of both sexes [...] Read more.
The differential contribution of monocyte subsets expressing the C-C chemokine receptor 2 (CCR2) to subclinical atherosclerosis in girls and boys is unclear. In this pilot study, we compared classical, intermediate, and nonclassical monocyte subsets expressing CCR2 in 33 obese children of both sexes aged 8 to 16 divided by carotid intima-media thickness (IMT), considering values above the 75th percentile (p75) as abnormally high IMT. Obesity was defined as body mass index above the 95th percentile according to age and sex. Flow cytometry analyses revealed that boys but not girls with IMT ≥ p75 displayed increased CCR2+ cell percentage and CCR2 expression in the three monocyte subsets, compared to boys with IMT < p75. The CCR2+ cell percentage and CCR2 expression in the three monocyte subsets significantly correlated with increased IMT and insulin resistance in boys but not girls, where the CCR2+ nonclassical monocyte percentage had the strongest associations (r = 0.73 and r = 0.72, respectively). The role of CCR2+ monocyte subpopulations in identifying an abnormally high IMT shows a marked sexual dimorphism, where boys seem to be at higher subclinical atherosclerosis risk than girls. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiac Damage and Healing)
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17 pages, 1846 KiB  
Article
Amniotic Fluid microRNA in Severe Twin-Twin Transfusion Syndrome Cardiomyopathy—Identification of Differences and Predicting Demise
by Eleanor L. Schuchardt, Shelley D. Miyamoto, Timothy Crombleholme, Anis Karimpour-Fard, Armin Korst, Bonnie Neltner, Lisa W. Howley, Bettina Cuneo and Carmen C. Sucharov
J. Cardiovasc. Dev. Dis. 2022, 9(2), 37; https://doi.org/10.3390/jcdd9020037 - 23 Jan 2022
Cited by 3 | Viewed by 2859
Abstract
Twin-twin transfusion syndrome (TTTS) is a rare but serious cause of fetal cardiomyopathy with poorly understood pathophysiology and challenging prognostication. This study sought a nonbiased, comprehensive assessment of amniotic fluid (AF) microRNAs from TTTS pregnancies and associations of these miRNAs with clinical characteristics. [...] Read more.
Twin-twin transfusion syndrome (TTTS) is a rare but serious cause of fetal cardiomyopathy with poorly understood pathophysiology and challenging prognostication. This study sought a nonbiased, comprehensive assessment of amniotic fluid (AF) microRNAs from TTTS pregnancies and associations of these miRNAs with clinical characteristics. For the discovery cohort, AF from ten fetuses with severe TTTS cardiomyopathy were selected and compared to ten normal singleton AF. Array panels assessing 384 microRNAs were performed on the discovery cohort and controls. Using a stringent q < 0.0025, arrays identified 32 miRNAs with differential expression. Top three microRNAs were miR-99b, miR-370 and miR-375. Forty distinct TTTS subjects were selected for a validation cohort. RT-PCR targeted six differentially-expressed microRNAs in the discovery and validation cohorts. Expression differences by array were confirmed by RT-PCR with high fidelity. The ability of these miRNAs to predict clinical differences, such as cardiac findings and later demise, was evaluated on TTTS subjects. Down-regulation of miRNA-127-3p, miRNA-375-3p and miRNA-886 were associated with demise. Our results indicate AF microRNAs have potential as a diagnostic and prognostic biomarker in TTTS. The top microRNAs have previously demonstrated roles in angiogenesis, cardiomyocyte stress response and hypertrophy. Further studies of the mechanism of actions and potential targets is warranted. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiac Damage and Healing)
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Review

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12 pages, 533 KiB  
Review
Review of Recent Laboratory and Experimental Data on Cardiotoxicity of Statins
by Aleksey M. Chaulin
J. Cardiovasc. Dev. Dis. 2022, 9(11), 403; https://doi.org/10.3390/jcdd9110403 - 19 Nov 2022
Cited by 3 | Viewed by 1300
Abstract
Due to the fact that statins are among the most high-demand therapeutic agents used for the treatment and prevention of the most common cardiovascular diseases, a significant amount of research is focused on these drugs. As a result, the study and discovery of [...] Read more.
Due to the fact that statins are among the most high-demand therapeutic agents used for the treatment and prevention of the most common cardiovascular diseases, a significant amount of research is focused on these drugs. As a result, the study and discovery of new effects in statin drugs continues. Research methods are constantly being improved in terms of their sensitivity and specificity, which leads to a change in ideas. In addition to the main lipid-lowering effect, statins have a number of additional effects, which can be conditionally divided into positive (pleiotropic) and negative (side effects). Moreover, information about many of the pleiotropic effects of statins is controversial and may subsequently change as new data become available. To a large extent, this is due to the introduction of new and the improvement of old methods of study: clinical, laboratory and morphological ones. Recent studies report the possibility of statins having potential cardiotoxic properties, which is expressed by an increase in the concentration of highly sensitive cardiac troponins, as well as various adverse changes in cardiac myocytes at the ultrastructural and molecular levels. This paper discusses possible mechanisms of statin cardiotoxicity. This narrative review is based on an analysis of publications in the Medline, PubMed, PubMed Central and Embase databases. The terms “statins”, “troponin”, “troponin I”, “troponin T” in combination with “cardiotoxicity”, “false positive”, “mechanisms of increase”, “pathophysiological mechanisms”, “oxidative stress” and “cardiomyocyte apoptosis” were used to search publications. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Cardiac Damage and Healing)
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