Molecular Signaling and Cellular Mechanisms in Cardiac Tissue Repair, Remodeling and Fibrosis

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

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 1915

Special Issue Editor


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Guest Editor
Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA
Interests: mechanisms in cardiac fibrosis and remodeling; myocardial infarction; intracardiac dopamine receptors; cardiac collagen turnover; vasoactive peptides

Special Issue Information

Dear Colleagues,

We are thrilled to announce a Special Issue entitled “Molecular Signaling and Cellular Mechanisms in Cardiac Tissue Repair, Remodeling and Fibrosis”. This Special Issue aims to provide a comprehensive overview of the molecular signaling pathways and cellular mechanisms involved in cardiac tissue repair, remodeling and fibrosis.

The extracellular matrix is a vital part of cardiac tissue that gives the heart the physical and mechanical means to be able to function properly. The structure of the ECM is extremely dynamic and the composition and formation change to accommodate changes to the body and organ systems. However, it may develop out of control, resulting in altered tissue properties and function. Fibrosis can impair cardiac function and lead to the development of arrhythmias, heart failure and sudden cardiac death, all of which contribute to the leading cause of death in the world. There are several molecular signaling pathways, cellular mechanisms and risk factors that can contribute to cardiac tissue remodeling and fibrosis, such as the many mediators that are involved in the recruitment and activation of cell types into myofibroblasts that are responsible for ferocious ECM secretions. This Special Issue will focus on the latest research findings related to the signaling pathways and mechanisms involved in this complex development of fibrosis and distinguishing targets and therapeutics that can help reverse or mitigate fibrosis and improve cardiac structure and function.  

The papers in this Special Issue will focus on the latest research findings related to the molecular signaling pathways, cellular mechanisms and risk factors that contribute to cardiac tissue remodeling and fibrosis. Topics covered will include, but not be limited to:

  • Signaling pathways involved in fibrosis;
  • Role of the cardiac fibroblast and myofibroblast in remodeling;
  • Transcriptional regulation of collagen expression;
  • Cleaved peptides in fibroblast extracellular matrix regulation;
  • Molecular alterations to cardiac structure and function;
  • Mitigation or reversal of cardiac injury/fibrosis.

Overall, this Special Issue promises to be an essential resource for cardiovascular scientists and clinicians interested in gaining a better understanding of the molecular signaling and cellular mechanisms underlying cardiac tissue remodeling and fibrosis.  Our goal is to provide a platform for the dissemination of cutting-edge research in this important area of cardiovascular research.

We welcome original research articles, reviews, communications and perspectives from researchers in all areas of cardiovascular biology, including basic science and translational research. We look forward to your contributions!

Dr. Laxmansa C. Katwa
Guest Editor

Manuscript Submission Information

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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
  • heart failure
  • hypertension
  • fibrosis
  • extracellular matrix
  • cardiac fibroblast/myofibroblast
  • collagen
  • cardiac injury
  • myocardial infarction

Published Papers (1 paper)

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Review

14 pages, 956 KiB  
Review
The Eye of the Storm: Investigating the Long-Term Cardiovascular Effects of COVID-19 and Variants
by Nandini Vishwakarma, Reshma B. Goud, Myna Prakash Tirupattur and Laxmansa C. Katwa
Cells 2023, 12(17), 2154; https://doi.org/10.3390/cells12172154 - 27 Aug 2023
Cited by 1 | Viewed by 1555
Abstract
COVID-19 had stormed through the world in early March of 2019, and on 5 May 2023, SARS-CoV-2 was officially declared to no longer be a global health emergency. The rise of new COVID-19 variants XBB.1.5 and XBB.1.16, a product of recombinant variants [...] Read more.
COVID-19 had stormed through the world in early March of 2019, and on 5 May 2023, SARS-CoV-2 was officially declared to no longer be a global health emergency. The rise of new COVID-19 variants XBB.1.5 and XBB.1.16, a product of recombinant variants and sub-strains, has fueled a need for continued surveillance of the pandemic as they have been deemed increasingly infectious. Regardless of the severity of the variant, this has caused an increase in hospitalizations, a strain in resources, and a rise of concern for public health. In addition, there is a growing population of patients experiencing cardiovascular complications as a result of post-acute sequelae of COVID-19. This review aims to focus on what was known about SARS-CoV-2 and its past variants (Alpha, Delta, Omicron) and how the knowledge has grown today with new emerging variants, with an emphasis on cardiovascular complexities. We focus on the possible mechanisms that cause the observations of chronic cardiac conditions seen even after patients have recovered from the infection. Further understanding of these mechanisms will help to close the gap in knowledge on post-acute sequelae of COVID-19 and the differences between the effects of variants. Full article
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