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

Michael J Daseke 2nd; Mavis A A Tenkorang; Upendra Chalise; Shelby R Konfrst; Merry L Lindsey

doi:10.1016/j.matbio.2020.03.010

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

Matrix Biol. 2020 Sep:91-92:109-116. doi: 10.1016/j.matbio.2020.03.010. Epub 2020 May 21.

Authors

Michael J Daseke 2nd¹, Mavis A A Tenkorang², Upendra Chalise², Shelby R Konfrst², Merry L Lindsey³

Affiliations

¹ Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, 985850 Nebraska Medical Center Omaha, NE 68198-5850, USA; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, 39216, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA.
² Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, 985850 Nebraska Medical Center Omaha, NE 68198-5850, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA.
³ Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, 985850 Nebraska Medical Center Omaha, NE 68198-5850, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA. Electronic address: Merry.Lindsey@unmc.edu.

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.

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

Publication types

Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Review

MeSH terms

Animals
Cell Differentiation
Cell Lineage / genetics
Cytokines / genetics
Cytokines / metabolism
Extracellular Matrix / chemistry
Extracellular Matrix / metabolism*
Extracellular Matrix / pathology
Extracellular Matrix Proteins / genetics*
Extracellular Matrix Proteins / metabolism
Fibroblasts / classification
Fibroblasts / metabolism*
Fibroblasts / pathology
Gene Expression Regulation
Humans
Mice
Myocardial Infarction / genetics
Myocardial Infarction / metabolism*
Myocardial Infarction / pathology
Myocardial Infarction / rehabilitation
Myocardium / metabolism
Myocardium / pathology
Recovery of Function / genetics*
Signal Transduction
Transforming Growth Factor beta / genetics
Transforming Growth Factor beta / metabolism
Vascular Endothelial Growth Factor A / genetics
Vascular Endothelial Growth Factor A / metabolism
Wound Healing / physiology

Substances

Cytokines
Extracellular Matrix Proteins
Transforming Growth Factor beta
VEGFA protein, human
Vascular Endothelial Growth Factor A

Abstract

Publication types

MeSH terms

Substances

Grants and funding