Research on Cell Plasticity and Tissue Remodeling in the Cardiovascular System

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Clinical Medicine, Cell, and Organism Physiology".

Deadline for manuscript submissions: closed (1 October 2021) | Viewed by 8431

Special Issue Editor


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Guest Editor
College of Engineering, Michigan State University, East Lansing, MI, USA
Interests: gene expression; cell signaling; cell biology; cell culture; flow cytometry; stem cell biology; tissue engineering; genetics; molecular biology; biochemistry

Special Issue Information

Dear Colleagues,

Background: Cardiovascular disease constitutes the main cause of death in the developed world. Treatment options are very limited and typically focus on the management of symptoms. Remodeling of the cardiovascular system upon injury constitutes a critical step in disease progression and can mark the difference between complete regeneration/repair or pathological remodeling. It is critical to understand the mechanisms of cell plasticity and tissue remodeling in the damaged cardiovascular system to develop new and personalized therapeutic approaches.

Aims and scope: The aim of this Special Issue is to present a collection of original research articles and comprehensive reviews focusing on:

  • Mechanisms of cardiac regeneration (including but not limited to cardiac stem cells, epigenetic mechanisms, and in vivo reprogramming);
  • Mechanisms of pathologic vascular remodeling (atherosclerotic plaque development, endothelial-to-mesenchymal transition, and stenosis);
  • Novel therapeutic development for cardiovascular regeneration or to prevent pathologic remodeling;
  • Inflammation and its role in promoting and stopping pathological cardiovascular tissue remodeling.

History: Over the last two decades, it has become increasingly clear that the cardiovascular system is not quiescent and contains significant populations of progenitor cells to undergo repair and homeostasis. We have also learned that mature cells, such as cardiomyocytes or endothelial cells, possess a certain degree of plasticity, allowing them to dedifferentiate and/or transdifferentiate into other related cell types. These homeostatic remodeling mechanisms play important roles when the cardiovascular tissue is damaged or as we age, and can contribute very significantly to pathological remodeling and disease progression.

Cutting-edge research: We are inviting submissions on cutting-edge research investigating mechanisms of cell plasticity and tissue remodeling in the cardiovascular system, or dealing with novel therapeutics aimed at modulating these tissue remodeling pathways.

What kind of papers we are soliciting: We are looking for original research articles and comprehensive reviews focusing on the last decade of advances on this topic. 

Dr. Aitor Aguirre
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. Journal of Personalized Medicine 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 2600 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
  • stem cells
  • cell reprogramming
  • cell plasticity
  • regeneration
  • inflammation
  • tissue remodeling
  • epigenetic
  • endothelial
  • in vivo reprogramming

Published Papers (2 papers)

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Research

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21 pages, 7029 KiB  
Article
In Situ Maturated Early-Stage Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes Improve Cardiac Function by Enhancing Segmental Contraction in Infarcted Rats
by Diogo Biagi, Evelyn Thais Fantozzi, Julliana Carvalho Campos-Oliveira, Marcus Vinicius Naghetini, Antonio Fernando Ribeiro, Jr., Sirlene Rodrigues, Isabella Ogusuku, Rubia Vanderlinde, Michelle Lopes Araújo Christie, Debora Bastos Mello, Antonio Carlos Campos de Carvalho, Marcos Valadares, Estela Cruvinel and Rafael Dariolli
J. Pers. Med. 2021, 11(5), 374; https://doi.org/10.3390/jpm11050374 - 4 May 2021
Cited by 8 | Viewed by 3774
Abstract
The scant ability of cardiomyocytes to proliferate makes heart regeneration one of the biggest challenges of science. Current therapies do not contemplate heart re-muscularization. In this scenario, stem cell-based approaches have been proposed to overcome this lack of regeneration. We hypothesize that early-stage [...] Read more.
The scant ability of cardiomyocytes to proliferate makes heart regeneration one of the biggest challenges of science. Current therapies do not contemplate heart re-muscularization. In this scenario, stem cell-based approaches have been proposed to overcome this lack of regeneration. We hypothesize that early-stage hiPSC-derived cardiomyocytes (hiPSC-CMs) could enhance the cardiac function of rats after myocardial infarction (MI). Animals were subjected to the permanent occlusion of the left ventricle (LV) anterior descending coronary artery (LAD). Seven days after MI, early-stage hiPSC-CMs were injected intramyocardially. Rats were subjected to echocardiography pre-and post-treatment. Thirty days after the injections were administered, treated rats displayed 6.2% human cardiac grafts, which were characterized molecularly. Left ventricle ejection fraction (LVEF) was improved by 7.8% in cell-injected rats, while placebo controls showed an 18.2% deterioration. Additionally, cell-treated rats displayed a 92% and 56% increase in radial and circumferential strains, respectively. Human cardiac grafts maturate in situ, preserving proliferation with 10% Ki67 and 3% PHH3 positive nuclei. Grafts were perfused by host vasculature with no evidence for immune rejection nor ectopic tissue formations. Our findings support the use of early-stage hiPSC-CMs as an alternative therapy to treat MI. The next steps of preclinical development include efficacy studies in large animals on the path to clinical-grade regenerative therapy targeting human patients. Full article
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21 pages, 2204 KiB  
Review
The Endothelium as a Target for Anti-Atherogenic Therapy: A Focus on the Epigenetic Enzymes EZH2 and SIRT1
by Jolien Fledderus, Byambasuren Vanchin, Marianne G. Rots and Guido Krenning
J. Pers. Med. 2021, 11(2), 103; https://doi.org/10.3390/jpm11020103 - 5 Feb 2021
Cited by 18 | Viewed by 4104
Abstract
Endothelial cell inflammatory activation and dysfunction are key events in the pathophysiology of atherosclerosis, and are associated with an elevated risk of cardiovascular events. Yet, therapies specifically targeting the endothelium and atherosclerosis are lacking. Here, we review how endothelial behaviour affects atherogenesis and [...] Read more.
Endothelial cell inflammatory activation and dysfunction are key events in the pathophysiology of atherosclerosis, and are associated with an elevated risk of cardiovascular events. Yet, therapies specifically targeting the endothelium and atherosclerosis are lacking. Here, we review how endothelial behaviour affects atherogenesis and pose that the endothelium may be an efficacious cellular target for antiatherogenic therapies. We discuss the contribution of endothelial inflammatory activation and dysfunction to atherogenesis and postulate that the dysregulation of specific epigenetic enzymes, EZH2 and SIRT1, aggravate endothelial dysfunction in a pleiotropic fashion. Moreover, we propose that commercially available drugs are available to clinically explore this postulation. Full article
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