Cardiac macrophages adopt profibrotic/M2 phenotype in infarcted hearts: Role of urokinase plasminogen activator
- 1 June 2016
- journal article
- Published by Elsevier BV in Journal of Molecular and Cellular Cardiology
- Vol. 108, 42-49
- https://doi.org/10.1016/j.yjmcc.2016.05.016
Abstract
No abstract availableKeywords
Funding Information
- Tall Family Foundation
This publication has 32 references indexed in Scilit:
- Prednisolone as Preservation Additive Prevents from Ischemia Reperfusion Injury in a Rat Model of Orthotopic Lung TransplantationPLOS ONE, 2013
- Urokinase Plasminogen Activator Induces Pro-Fibrotic/M2 Phenotype in Murine Cardiac MacrophagesPLOS ONE, 2013
- Matrix Metalloproteinase-28 Deletion Exacerbates Cardiac Dysfunction and Rupture After Myocardial Infarction in Mice by Inhibiting M2 Macrophage ActivationCirculation Research, 2013
- Protective and pathogenic functions of macrophage subsetsNature Reviews Immunology, 2011
- Cardiac mesenchymal stem cells contribute to scar formation after myocardial infarctionCardiovascular Research, 2011
- The role of macrophage-derived urokinase plasminogen activator in myocardial infarct repair: Urokinase attenuates ventricular remodelingJournal of Molecular and Cellular Cardiology, 2010
- Alternative Activation of Macrophages: Mechanism and FunctionsImmunity, 2010
- The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functionsThe Journal of Experimental Medicine, 2007
- Monocyte and macrophage heterogeneityNature Reviews Immunology, 2005
- Overexpression of Urokinase by Macrophages or Deficiency of Plasminogen Activator Inhibitor Type 1 Causes Cardiac Fibrosis in MiceCirculation Research, 2004