000163396 001__ 163396
000163396 005__ 20240320115517.0
000163396 0247_ $$2doi$$a10.1016/j.cmet.2021.10.004
000163396 0247_ $$2pmid$$apmid:34715039
000163396 0247_ $$2ISSN$$a1550-4131
000163396 0247_ $$2ISSN$$a1932-7420
000163396 0247_ $$2altmetric$$aaltmetric:115903501
000163396 037__ $$aDZNE-2022-00158
000163396 041__ $$aEnglish
000163396 082__ $$a570
000163396 1001_ $$aWillenborg, Sebastian$$b0
000163396 245__ $$aMitochondrial metabolism coordinates stage-specific repair processes in macrophages during wound healing.
000163396 260__ $$aCambridge, Mass.$$bCell Press$$c2021
000163396 3367_ $$2DRIVER$$aarticle
000163396 3367_ $$2DataCite$$aOutput Types/Journal article
000163396 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1654853378_23357
000163396 3367_ $$2BibTeX$$aARTICLE
000163396 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000163396 3367_ $$00$$2EndNote$$aJournal Article
000163396 500__ $$a(CC BY)
000163396 520__ $$aWound healing is a coordinated process that initially relies on pro-inflammatory macrophages, followed by a pro-resolution function of these cells. Changes in cellular metabolism likely dictate these distinct activities, but the nature of these changes has been unclear. Here, we profiled early- versus late-stage skin wound macrophages in mice at both the transcriptional and functional levels. We found that glycolytic metabolism in the early phase is not sufficient to ensure productive repair. Instead, by combining conditional disruption of the electron transport chain with deletion of mitochondrial aspartyl-tRNA synthetase, followed by single-cell sequencing analysis, we found that a subpopulation of early-stage wound macrophages are marked by mitochondrial ROS (mtROS) production and HIF1α stabilization, which ultimately drives a pro-angiogenic program essential for timely healing. In contrast, late-phase, pro-resolving wound macrophages are marked by IL-4Rα-mediated mitochondrial respiration and mitohormesis. Collectively, we identify changes in mitochondrial metabolism as a critical control mechanism for macrophage effector functions during wound healing.
000163396 536__ $$0G:(DE-HGF)POF4-354$$a354 - Disease Prevention and Healthy Aging (POF4-354)$$cPOF4-354$$fPOF IV$$x0
000163396 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000163396 650_7 $$2Other$$ametabolism
000163396 650_7 $$2Other$$amitochondria
000163396 650_7 $$2Other$$amitochondrial repurposing
000163396 650_7 $$2Other$$amitohormesis
000163396 650_7 $$2Other$$amonocyte/macrophage
000163396 650_7 $$2Other$$atissue repair
000163396 650_7 $$2Other$$atype 2 immunity
000163396 650_7 $$2Other$$awound healing
000163396 650_2 $$2MeSH$$aAnimals
000163396 650_2 $$2MeSH$$aMacrophages: metabolism
000163396 650_2 $$2MeSH$$aMice
000163396 650_2 $$2MeSH$$aMitochondria: metabolism
000163396 650_2 $$2MeSH$$aWound Healing
000163396 7001_ $$aSanin, David E$$b1
000163396 7001_ $$aJais, Alexander$$b2
000163396 7001_ $$aDing, Xiaolei$$b3
000163396 7001_ $$0P:(DE-2719)9000845$$aUlas, Thomas$$b4$$udzne
000163396 7001_ $$aNüchel, Julian$$b5
000163396 7001_ $$aPopović, Milica$$b6
000163396 7001_ $$aMacVicar, Thomas$$b7
000163396 7001_ $$aLanger, Thomas$$b8
000163396 7001_ $$0P:(DE-2719)2811660$$aSchultze, Joachim L$$b9$$udzne
000163396 7001_ $$aGerbaulet, Alexander$$b10
000163396 7001_ $$aRoers, Axel$$b11
000163396 7001_ $$aPearce, Edward J$$b12
000163396 7001_ $$aBrüning, Jens C$$b13
000163396 7001_ $$aTrifunovic, Aleksandra$$b14
000163396 7001_ $$aEming, Sabine A$$b15
000163396 773__ $$0PERI:(DE-600)2174469-5$$a10.1016/j.cmet.2021.10.004$$gVol. 33, no. 12, p. 2398 - 2414.e9$$n12$$p2398 - 2414.e9$$tCell metabolism$$v33$$x1550-4131$$y2021
000163396 8564_ $$uhttps://pub.dzne.de/record/163396/files/DZNE-2022-00158.pdf$$yOpenAccess
000163396 8564_ $$uhttps://pub.dzne.de/record/163396/files/DZNE-2022-00158.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000163396 909CO $$ooai:pub.dzne.de:163396$$pdnbdelivery$$pdriver$$popenaire$$pVDB$$popen_access
000163396 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9000845$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b4$$kDZNE
000163396 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811660$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b9$$kDZNE
000163396 9131_ $$0G:(DE-HGF)POF4-354$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Prevention and Healthy Aging$$x0
000163396 9141_ $$y2021
000163396 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2021-02-03
000163396 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000163396 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bCELL METAB : 2021$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)9930$$2StatID$$aIF >= 30$$bCELL METAB : 2021$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2021-02-03
000163396 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000163396 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2022-11-22
000163396 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2021-02-03
000163396 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2022-11-22
000163396 9201_ $$0I:(DE-2719)1013031$$kAG Schultze$$lUnited epigenomic platform$$x0
000163396 980__ $$ajournal
000163396 980__ $$aVDB
000163396 980__ $$aUNRESTRICTED
000163396 980__ $$aI:(DE-2719)1013031
000163396 9801_ $$aFullTexts