The Elusive Antifibrotic Macrophage

Fibrotic diseases, especially of the liver, the cardiovascular system, the kidneys, and the lungs, account for approximately 45% of deaths in Western societies. Fibrosis is a serious complication associated with aging and/or chronic inflammation or injury and cannot be treated effectively yet. It is...

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Main Authors:	Adhyatmika, Adhyatmika, Putri, Kurnia S. S., Beljaars, Leonie, Melgert, Barbro N.
Format:	Online
Language:	English
Published:	Frontiers Media S.A. 2015
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4643133/

id	pubmed-4643133
recordtype	oai_dc
spelling	pubmed-46431332015-11-27 The Elusive Antifibrotic Macrophage Adhyatmika, Adhyatmika Putri, Kurnia S. S. Beljaars, Leonie Melgert, Barbro N. Medicine Fibrotic diseases, especially of the liver, the cardiovascular system, the kidneys, and the lungs, account for approximately 45% of deaths in Western societies. Fibrosis is a serious complication associated with aging and/or chronic inflammation or injury and cannot be treated effectively yet. It is characterized by excessive deposition of extracellular matrix (ECM) proteins by myofibroblasts and impaired degradation by macrophages. This ultimately destroys the normal structure of an organ, which leads to loss of function. Most efforts to develop drugs have focused on inhibiting ECM production by myofibroblasts and have not yielded many effective drugs yet. Another option is to stimulate the cells that are responsible for degradation and uptake of excess ECM, i.e., antifibrotic macrophages. However, macrophages are plastic cells that have many faces in fibrosis, including profibrotic behavior-stimulating ECM production. This can be dependent on their origin, as the different organs have tissue-resident macrophages with different origins and a various influx of incoming monocytes in steady-state conditions and during fibrosis. To be able to pharmacologically stimulate the right kind of behavior in fibrosis, a thorough characterization of antifibrotic macrophages is necessary, as well as an understanding of the signals they need to degrade ECM. In this review, we will summarize the current state of the art regarding the antifibrotic macrophage phenotype and the signals that stimulate its behavior. Frontiers Media S.A. 2015-11-13 /pmc/articles/PMC4643133/ /pubmed/26618160 http://dx.doi.org/10.3389/fmed.2015.00081 Text en Copyright © 2015 Adhyatmika, Putri, Beljaars and Melgert. 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) or licensor 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.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Adhyatmika, Adhyatmika Putri, Kurnia S. S. Beljaars, Leonie Melgert, Barbro N.
spellingShingle	Adhyatmika, Adhyatmika Putri, Kurnia S. S. Beljaars, Leonie Melgert, Barbro N. The Elusive Antifibrotic Macrophage
author_facet	Adhyatmika, Adhyatmika Putri, Kurnia S. S. Beljaars, Leonie Melgert, Barbro N.
author_sort	Adhyatmika, Adhyatmika
title	The Elusive Antifibrotic Macrophage
title_short	The Elusive Antifibrotic Macrophage
title_full	The Elusive Antifibrotic Macrophage
title_fullStr	The Elusive Antifibrotic Macrophage
title_full_unstemmed	The Elusive Antifibrotic Macrophage
title_sort	elusive antifibrotic macrophage
description	Fibrotic diseases, especially of the liver, the cardiovascular system, the kidneys, and the lungs, account for approximately 45% of deaths in Western societies. Fibrosis is a serious complication associated with aging and/or chronic inflammation or injury and cannot be treated effectively yet. It is characterized by excessive deposition of extracellular matrix (ECM) proteins by myofibroblasts and impaired degradation by macrophages. This ultimately destroys the normal structure of an organ, which leads to loss of function. Most efforts to develop drugs have focused on inhibiting ECM production by myofibroblasts and have not yielded many effective drugs yet. Another option is to stimulate the cells that are responsible for degradation and uptake of excess ECM, i.e., antifibrotic macrophages. However, macrophages are plastic cells that have many faces in fibrosis, including profibrotic behavior-stimulating ECM production. This can be dependent on their origin, as the different organs have tissue-resident macrophages with different origins and a various influx of incoming monocytes in steady-state conditions and during fibrosis. To be able to pharmacologically stimulate the right kind of behavior in fibrosis, a thorough characterization of antifibrotic macrophages is necessary, as well as an understanding of the signals they need to degrade ECM. In this review, we will summarize the current state of the art regarding the antifibrotic macrophage phenotype and the signals that stimulate its behavior.
publisher	Frontiers Media S.A.
publishDate	2015
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4643133/
_version_	1613500594657427456

The Elusive Antifibrotic Macrophage

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