Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction

Yonggang Ma, Alan J. Mouton, Merry L. Lindsey

Research output: Contribution to journalReview article

38 Citations (Scopus)

Abstract

Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady-state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a proinflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both proinflammatory and anti-inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a proinflammatory M1 phenotype early and become polarized toward an anti-inflammatory M2 phenotype later post-MI. Although this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.

Original languageEnglish (US)
Pages (from-to)15-28
Number of pages14
JournalTranslational Research
Volume191
DOIs
StatePublished - Jan 2018

Fingerprint

Macrophages
Aging of materials
Myocardial Infarction
Phenotype
Anti-Inflammatory Agents
Matrix Metalloproteinases
Chemokines
Cicatrix
Intercellular Signaling Peptides and Proteins
Myocardium
Repair
Maintenance
Polarization
Tissue
Cytokines
Wounds and Injuries

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Biochemistry, medical

Cite this

Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction. / Ma, Yonggang; Mouton, Alan J.; Lindsey, Merry L.

In: Translational Research, Vol. 191, 01.2018, p. 15-28.

Research output: Contribution to journalReview article

@article{14c19669bcae4c9abb116d56a6557bf7,
title = "Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction",
abstract = "Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady-state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a proinflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both proinflammatory and anti-inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a proinflammatory M1 phenotype early and become polarized toward an anti-inflammatory M2 phenotype later post-MI. Although this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.",
author = "Yonggang Ma and Mouton, {Alan J.} and Lindsey, {Merry L.}",
year = "2018",
month = "1",
doi = "10.1016/j.trsl.2017.10.001",
language = "English (US)",
volume = "191",
pages = "15--28",
journal = "Translational Research",
issn = "1931-5244",
publisher = "Mosby Inc.",

}

TY - JOUR

T1 - Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction

AU - Ma, Yonggang

AU - Mouton, Alan J.

AU - Lindsey, Merry L.

PY - 2018/1

Y1 - 2018/1

N2 - Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady-state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a proinflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both proinflammatory and anti-inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a proinflammatory M1 phenotype early and become polarized toward an anti-inflammatory M2 phenotype later post-MI. Although this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.

AB - Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady-state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a proinflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both proinflammatory and anti-inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a proinflammatory M1 phenotype early and become polarized toward an anti-inflammatory M2 phenotype later post-MI. Although this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.

UR - http://www.scopus.com/inward/record.url?scp=85032890866&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85032890866&partnerID=8YFLogxK

U2 - 10.1016/j.trsl.2017.10.001

DO - 10.1016/j.trsl.2017.10.001

M3 - Review article

C2 - 29106912

AN - SCOPUS:85032890866

VL - 191

SP - 15

EP - 28

JO - Translational Research

JF - Translational Research

SN - 1931-5244

ER -