TY - JOUR
T1 - Abandoning M1/M2 for a network model of macrophage function
AU - Nahrendorf, Matthias
AU - Swirski, Filip K.
N1 - Publisher Copyright:
© 2016 American Heart Association, Inc.
PY - 2016/7/22
Y1 - 2016/7/22
N2 - 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.
AB - 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.
KW - atherosclerosis
KW - bone marrow
KW - macrophage
KW - monocyte
KW - myocardial infarction
UR - http://www.scopus.com/inward/record.url?scp=84979582060&partnerID=8YFLogxK
U2 - 10.1161/CIRCRESAHA.116.309194
DO - 10.1161/CIRCRESAHA.116.309194
M3 - Review article
C2 - 27458196
AN - SCOPUS:84979582060
SN - 0009-7330
VL - 119
SP - 414
EP - 417
JO - Circulation Research
JF - Circulation Research
IS - 3
ER -