Mitochondrial Dysfunction Prevents Repolarization of Inflammatory Macrophages
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- 作者：Jan Van den Bossche1 ; 5 ; j.vandenbossche@amc.uva.nl" class="auth_mail" title="E-mail the corresponding author ; Jeroen Baardman1 ; Natasja A. Otto1 ; 2 ; 3 ; Saskia van der Velden1 ; Annette E. Neele1 ; Susan M. van den Berg1 ; Rosario Luque-Martin1 ; Hung-Jen Chen1 ; Marieke C.S. Boshuizen1 ; Mohamed Ahmed1 ; Marten A. Hoeksema1 ; Alex F. de Vos2 ; 3 ; Menno P.J. de Winther1 ; 4
- 关键词：immunometabolism ; macrophage polarization ; macrophage plasticity ; metabolism ; inflammation ; metabolism ; mitochondrial dysfunction ; M1 M2 polarization ; alternative macrophage activation ; macrophage repolarization
- 刊名：Cell Reports
- 出版年：2016
- 出版时间：11 October 2016
- 年：2016
- 卷：17
- 期：3
- 页码：684-696
- 全文大小：3570 K
文摘
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Mouse and human M1 macrophages fail to repolarize to M2 upon IL-4 restimulation
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LPS + IFNγ treatment inhibits mitochondrial oxidative respiration in macrophages
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Mitochondrial function is required for the repolarization to an M2 phenotype
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NO blunts mitochondrial respiration and prevents plasticity in M1 macrophages