Cargando…

Leukocyte-Dependent Regulation of Cardiac Fibrosis

Cardiac fibrosis begins as an intrinsic response to injury or ageing that functions to preserve the tissue from further damage. Fibrosis results from activated cardiac myofibroblasts, which secrete extracellular matrix (ECM) proteins in an effort to replace damaged tissue; however, excessive ECM dep...

Descripción completa

Detalles Bibliográficos
Autores principales: Okyere, Ama Dedo, Tilley, Douglas G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156539/
https://www.ncbi.nlm.nih.gov/pubmed/32322219
http://dx.doi.org/10.3389/fphys.2020.00301
_version_ 1783522230141976576
author Okyere, Ama Dedo
Tilley, Douglas G.
author_facet Okyere, Ama Dedo
Tilley, Douglas G.
author_sort Okyere, Ama Dedo
collection PubMed
description Cardiac fibrosis begins as an intrinsic response to injury or ageing that functions to preserve the tissue from further damage. Fibrosis results from activated cardiac myofibroblasts, which secrete extracellular matrix (ECM) proteins in an effort to replace damaged tissue; however, excessive ECM deposition leads to pathological fibrotic remodeling. At this extent, fibrosis gravely disturbs myocardial compliance, and ultimately leads to adverse outcomes like heart failure with heightened mortality. As such, understanding the complexity behind fibrotic remodeling has been a focal point of cardiac research in recent years. Resident cardiac fibroblasts and activated myofibroblasts have been proven integral to the fibrotic response; however, several findings point to additional cell types that may contribute to the development of pathological fibrosis. For one, leukocytes expand in number after injury and exhibit high plasticity, thus their distinct role(s) in cardiac fibrosis is an ongoing and controversial field of study. This review summarizes current findings, focusing on both direct and indirect leukocyte-mediated mechanisms of fibrosis, which may provide novel targeted strategies against fibrotic remodeling.
format Online
Article
Text
id pubmed-7156539
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-71565392020-04-22 Leukocyte-Dependent Regulation of Cardiac Fibrosis Okyere, Ama Dedo Tilley, Douglas G. Front Physiol Physiology Cardiac fibrosis begins as an intrinsic response to injury or ageing that functions to preserve the tissue from further damage. Fibrosis results from activated cardiac myofibroblasts, which secrete extracellular matrix (ECM) proteins in an effort to replace damaged tissue; however, excessive ECM deposition leads to pathological fibrotic remodeling. At this extent, fibrosis gravely disturbs myocardial compliance, and ultimately leads to adverse outcomes like heart failure with heightened mortality. As such, understanding the complexity behind fibrotic remodeling has been a focal point of cardiac research in recent years. Resident cardiac fibroblasts and activated myofibroblasts have been proven integral to the fibrotic response; however, several findings point to additional cell types that may contribute to the development of pathological fibrosis. For one, leukocytes expand in number after injury and exhibit high plasticity, thus their distinct role(s) in cardiac fibrosis is an ongoing and controversial field of study. This review summarizes current findings, focusing on both direct and indirect leukocyte-mediated mechanisms of fibrosis, which may provide novel targeted strategies against fibrotic remodeling. Frontiers Media S.A. 2020-04-08 /pmc/articles/PMC7156539/ /pubmed/32322219 http://dx.doi.org/10.3389/fphys.2020.00301 Text en Copyright © 2020 Okyere and Tilley. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Okyere, Ama Dedo
Tilley, Douglas G.
Leukocyte-Dependent Regulation of Cardiac Fibrosis
title Leukocyte-Dependent Regulation of Cardiac Fibrosis
title_full Leukocyte-Dependent Regulation of Cardiac Fibrosis
title_fullStr Leukocyte-Dependent Regulation of Cardiac Fibrosis
title_full_unstemmed Leukocyte-Dependent Regulation of Cardiac Fibrosis
title_short Leukocyte-Dependent Regulation of Cardiac Fibrosis
title_sort leukocyte-dependent regulation of cardiac fibrosis
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156539/
https://www.ncbi.nlm.nih.gov/pubmed/32322219
http://dx.doi.org/10.3389/fphys.2020.00301
work_keys_str_mv AT okyereamadedo leukocytedependentregulationofcardiacfibrosis
AT tilleydouglasg leukocytedependentregulationofcardiacfibrosis