Cardiac Fibroblasts and Cardiac Remodeling

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (30 December 2023) | Viewed by 1743

Special Issue Editor


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Guest Editor
Department of Physiology & Pharmacology, West Virginia University, Morgantown, WV, USA
Interests: how effector molecules interact with the immune system (including macrophages and mast cells, to induce cardiac fibrosis)

Special Issue Information

Dear Colleagues,

Cardiac fibrosis is defined as an aberrant excess accumulation of extracellular matrix (ECM), especially collagen, which results in the adverse remodeling of the heart. If remained untreated, this adverse cardiac remodeling will lead to organ dysfunction and ultimately organ failure, or, in this case, heart failure, which is one of the leading causes of death around the world. Whilst cardiac fibroblast is responsible for maintaining the overall structure and function of the heart, factors such as inflammation and tissue injury can trigger changes in cardiac fibroblast phenotype and function. This change not only includes the excess production of extracellular matrix (such as collagen, alpha smooth muscle actin, and laminin), but also the release of cytokines and chemokines, creating a profibrotic and proinflammatory environment, hence driving the adverse remodeling of the heart. 

This Special Issue of Cells aims to provide reviews and original research articles on the intricate role of cardiac fibroblasts, especially in cardiac remodeling. Articles on genetic and cellular functions, including both biochemical and mechanical aspects of cardiac fibroblasts, are highly welcome. 

Dr. Alexander Widiapradja
Guest Editor

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Keywords

  • fibroblasts
  • remodeling
  • fibrosis
  • ECM
  • cardiac fibrosis
  • cardiac remodeling

Published Papers (1 paper)

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Research

20 pages, 5250 KiB  
Article
Defining Transcriptomic Heterogeneity between Left and Right Ventricle-Derived Cardiac Fibroblasts
by Michael Bradley Dewar, Fahad Ehsan, Aliya Izumi, Hangjun Zhang, Yu-Qing Zhou, Haisam Shah, Dylan Langburt, Hamsini Suresh, Tao Wang, Alison Hacker, Boris Hinz, Jesse Gillis, Mansoor Husain and Scott Patrick Heximer
Cells 2024, 13(4), 327; https://doi.org/10.3390/cells13040327 - 10 Feb 2024
Viewed by 1511
Abstract
Cardiac fibrosis is a key aspect of heart failure, leading to reduced ventricular compliance and impaired electrical conduction in the myocardium. Various pathophysiologic conditions can lead to fibrosis in the left ventricle (LV) and/or right ventricle (RV). Despite growing evidence to support the [...] Read more.
Cardiac fibrosis is a key aspect of heart failure, leading to reduced ventricular compliance and impaired electrical conduction in the myocardium. Various pathophysiologic conditions can lead to fibrosis in the left ventricle (LV) and/or right ventricle (RV). Despite growing evidence to support the transcriptomic heterogeneity of cardiac fibroblasts (CFs) in healthy and diseased states, there have been no direct comparisons of CFs in the LV and RV. Given the distinct natures of the ventricles, we hypothesized that LV- and RV-derived CFs would display baseline transcriptomic differences that influence their proliferation and differentiation following injury. Bulk RNA sequencing of CFs isolated from healthy murine left and right ventricles indicated that LV-derived CFs may be further along the myofibroblast transdifferentiation trajectory than cells isolated from the RV. Single-cell RNA-sequencing analysis of the two populations confirmed that Postn+ CFs were more enriched in the LV, whereas Igfbp3+ CFs were enriched in the RV at baseline. Notably, following pressure overload injury, the LV developed a larger subpopulation of pro-fibrotic Thbs4+/Cthrc1+ injury-induced CFs, while the RV showed a unique expansion of two less-well-characterized CF subpopulations (Igfbp3+ and Inmt+). These findings demonstrate that LV- and RV-derived CFs display baseline subpopulation differences that may dictate their diverging responses to pressure overload injury. Further study of these subpopulations will elucidate their role in the development of fibrosis and inform on whether LV and RV fibrosis require distinct treatments. Full article
(This article belongs to the Special Issue Cardiac Fibroblasts and Cardiac Remodeling)
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