Literature DB >> 32446909

Cardiac fibroblast activation during myocardial infarction wound healing: Fibroblast polarization after MI.

Michael J Daseke1, Mavis A A Tenkorang2, Upendra Chalise2, Shelby R Konfrst2, Merry L Lindsey3.   

Abstract

Cardiac wound healing after myocardial infarction (MI) evolves from pro-inflammatory to anti-inflammatory to reparative responses, and the cardiac fibroblast is a central player during the entire transition. The fibroblast mirrors changes seen in the left ventricle infarct by undergoing a continuum of polarization phenotypes that follow pro-inflammatory, anti-inflammatory, and pro-scar producing profiles. The development of each phenotype transition is contingent upon the MI environment into which the fibroblast enters. In this mini-review, we summarize our current knowledge regarding cardiac fibroblast activation during MI and highlight key areas where gaps remain.
Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  fibroblast; inflammation; myocardial infarction; scar formation; wound healing

Year:  2020        PMID: 32446909      PMCID: PMC7434699          DOI: 10.1016/j.matbio.2020.03.010

Source DB:  PubMed          Journal:  Matrix Biol        ISSN: 0945-053X            Impact factor:   11.583


  71 in total

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Journal:  J Mol Cell Cardiol       Date:  1999-11       Impact factor: 5.000

2.  Altered fibroblast function following myocardial infarction.

Authors:  Christina E Squires; G Patricia Escobar; John F Payne; Robert A Leonardi; Danielle K Goshorn; Nina J Sheats; I Matthew Mains; Joseph T Mingoia; English C Flack; Merry L Lindsey
Journal:  J Mol Cell Cardiol       Date:  2005-10       Impact factor: 5.000

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4.  Targeting the renin-angiotensin-aldosterone system in fibrosis.

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Review 7.  Matrix metalloproteinase-9: Many shades of function in cardiovascular disease.

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Journal:  Mol Biol Cell       Date:  2017-05-03       Impact factor: 4.138

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  18 in total

Review 1.  Fibroblasts: The arbiters of extracellular matrix remodeling.

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Review 5.  Senescence mechanisms and targets in the heart.

Authors:  Maggie S Chen; Richard T Lee; Jessica C Garbern
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Review 6.  Fibroblast contributions to ischemic cardiac remodeling.

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7.  A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.

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8.  Targeting 5-HT2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After Myocardial Infarction.

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9.  Reperfused vs. nonreperfused myocardial infarction: when to use which model.

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Journal:  Am J Physiol Heart Circ Physiol       Date:  2021-06-11       Impact factor: 5.125

10.  Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension.

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