000141759 001__ 141759
000141759 005__ 20240229112526.0
000141759 0247_ $$2doi$$a10.1016/j.ajpath.2018.09.016
000141759 0247_ $$2pmid$$apmid:30448408
000141759 0247_ $$2ISSN$$a0002-9440
000141759 0247_ $$2ISSN$$a1525-2191
000141759 037__ $$aDKFZ-2018-02028
000141759 041__ $$aeng
000141759 082__ $$a610
000141759 1001_ $$aLux, Moritz$$b0
000141759 245__ $$aThe atypical chemokine receptor 2 limits progressive fibrosis after acute ischemic kidney injury.
000141759 260__ $$aNew York [u.a.]$$bElsevier$$c2019
000141759 3367_ $$2DRIVER$$aarticle
000141759 3367_ $$2DataCite$$aOutput Types/Journal article
000141759 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1552304946_14447
000141759 3367_ $$2BibTeX$$aARTICLE
000141759 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000141759 3367_ $$00$$2EndNote$$aJournal Article
000141759 520__ $$aFollowing renal ischemia-reperfusion injury (IRI) resolution of inflammation allows tubular regeneration, whereas ongoing inflammatory injury mediated by infiltrating leukocytes leads to nephron loss and renal fibrosis, typical hallmarks of chronic kidney disease. The atypical chemokine receptor 2 (ACKR2) is a chemokine decoy receptor, that binds and scavenges inflammatory CC-chemokines and reduces local leukocyte accumulation. We hypothesized that ACKR2 limits leukocyte infiltration, inflammation, and fibrotic tissue remodeling after renal IRI, thus preventing progression to chronic kidney disease. Compared to wild-type, Ackr2 deficiency increased CC chemokine ligand 2 levels in tumor necrosis factor-stimulated tubulointerstitial tissue in vitro. In Ackr2-deficient mice with early IRI one or five days after transient renal pedicle clamping tubular injury was similar to wild-type, although accumulation of mononuclear phagocytes increased in postischemic Ackr2-/- kidneys. Regarding long-term outcomes, Ackr2-/- kidneys displayed more tubular injury five weeks after IRI, which was associated with persistently increased renal infiltrates of mononuclear phagocytes, T cells, Ly6Chigh inflammatory macrophages, and inflammation. Moreover, Ackr2 deficiency resulted in substantially aggravated renal fibrosis in Ackr2-/- kidneys five weeks after IRI, as revealed by increased expression of matrix molecules, renal accumulation of αSMA+ myofibroblasts, and bone marrow-derived fibrocytes. ACKR2 plays an important role in limiting persistent inflammation, tubular loss, and renal fibrosis after ischemic acute kidney injury, and thus can prevent progression to chronic renal disease.
000141759 536__ $$0G:(DE-HGF)POF3-317$$a317 - Translational cancer research (POF3-317)$$cPOF3-317$$fPOF III$$x0
000141759 588__ $$aDataset connected to CrossRef, PubMed,
000141759 7001_ $$aBlaut, Alexander$$b1
000141759 7001_ $$aEltrich, Nuru$$b2
000141759 7001_ $$aBideak, Andrei$$b3
000141759 7001_ $$aMüller, Martin B$$b4
000141759 7001_ $$aHoppe, John M$$b5
000141759 7001_ $$0P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91$$aGröne, Hermann-Josef$$b6$$udkfz
000141759 7001_ $$aLocati, Massimo$$b7
000141759 7001_ $$aVielhauer, Volker$$b8
000141759 773__ $$0PERI:(DE-600)1480207-7$$a10.1016/j.ajpath.2018.09.016$$gp. S0002944017311495$$n2$$p231-247$$tThe American journal of pathology$$v189$$x0002-9440$$y2019
000141759 909CO $$ooai:inrepo02.dkfz.de:141759$$pVDB
000141759 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91$$aDeutsches Krebsforschungszentrum$$b6$$kDKFZ
000141759 9131_ $$0G:(DE-HGF)POF3-317$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vTranslational cancer research$$x0
000141759 9141_ $$y2019
000141759 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bAM J PATHOL : 2017
000141759 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000141759 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000141759 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000141759 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central
000141759 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List
000141759 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000141759 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000141759 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000141759 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine
000141759 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000141759 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000141759 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000141759 9201_ $$0I:(DE-He78)G130-20160331$$kG130$$lZelluläre und Molekulare Pathologie$$x0
000141759 980__ $$ajournal
000141759 980__ $$aVDB
000141759 980__ $$aI:(DE-He78)G130-20160331
000141759 980__ $$aUNRESTRICTED