Abandoning M1/M2 for a network model of macrophage function

Matthias Nahrendorf, Filip K. Swirski

Research output: Contribution to journalReview articlepeer-review

212 Scopus citations

Abstract

The heart and blood vessels of a healthy individual contain resident immune cells, the majority of which are macrophages that have seeded these organs early in the development. In the mouse, ≈ 10% of noncardiomyocytes are macrophages,1,2 and humans may have comparable numbers.1 After myocardial infarction, macrophage numbers increase in the heart through the combined effects of massive recruitment of bone marrowderived cells and local self-renewal.1,3 Likewise, in atherosclerosis, the chronic lipiddriven inflammatory disease that is the underlying cause of myocardial infarction, macrophage numbers increase in the vessel wall, again because of recruitment and local proliferation.4 Although many of these insights have been generated in mouse models, compelling evidence from genome-wide association studies have associated innate immunity mediators with myocardial infarction,5 whereas prospective human studies have shown that blood monocyte levels can predict cardiovascular events in patients.

Original languageEnglish
Pages (from-to)414-417
Number of pages4
JournalCirculation Research
Volume119
Issue number3
DOIs
StatePublished - 22 Jul 2016
Externally publishedYes

Keywords

  • atherosclerosis
  • bone marrow
  • macrophage
  • monocyte
  • myocardial infarction

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