Abandoning M1/M2 for a network model of macrophage function

Circulation Research

Volumn 119, Issue 3, 2016, Pages 414-417

  Nahrendorf, Matthias ^a   Swirski, Filip K ^a  

^a MASSACHUSETTS GENERAL HOSPITAL   (United States)

Author keywords

atherosclerosis; bone marrow; macrophage; monocyte; myocardial infarction

Indexed keywords

ARGINASE; ARGININE; CHEMOKINE RECEPTOR CCR2; COLONY STIMULATING FACTOR 1; GAMMA INTERFERON; GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR; INTERLEUKIN 1; INTERLEUKIN 10; INTERLEUKIN 12; INTERLEUKIN 23; INTERLEUKIN 4; INTERLEUKIN 6; MANNOSE RECEPTOR; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; ORNITHINE; STAT1 PROTEIN; STAT6 PROTEIN; TRANSFORMING GROWTH FACTOR BETA; TUMOR NECROSIS FACTOR ALPHA; CD11B ANTIGEN; GALECTIN 3;

ATHEROSCLEROSIS; CARDIOVASCULAR DISEASE; CELL PROLIFERATION; GENOME-WIDE ASSOCIATION STUDY; HEART INFARCTION; HUMAN; INFLAMMATORY DISEASE; MACROPHAGE FUNCTION; MICROGLIA; MOUSE MODEL; NONHUMAN; PERITONEUM MACROPHAGE; PRIORITY JOURNAL; REVIEW; ANIMAL; BIOLOGICAL MODEL; BLOOD; IMMUNOLOGY; MACROPHAGE; PATHOPHYSIOLOGY; PHYSIOLOGY;

ANIMALS; GALECTIN 3; HUMANS; MACROPHAGE-1 ANTIGEN; MACROPHAGES; MODELS, BIOLOGICAL; MYOCARDIAL INFARCTION;

EID: 84979582060     PISSN: 00097330     EISSN: 15244571     Source Type: Journal    
DOI: 10.1161/CIRCRESAHA.116.309194     Document Type: Review

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