Dihazi, Hassan

[["dc.bibliographiccitation.artnumber","1325"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Goligorsky, Michael S."],["dc.date.accessioned","2019-07-09T11:45:55Z"],["dc.date.available","2019-07-09T11:45:55Z"],["dc.date.issued","2018"],["dc.description.abstract","Sirtuins (SIRT) are ubiquitous histone and protein deacetylases and a member of this family, SIRT1, is the best-studied one. Its functions in endothelial cells encompass branching angiogenesis, activation of endothelial nitric oxide synthase, regulation of proapoptotic and proinflammatory pathways, among others. Defective SIRT1 activity has been described in various cardiovascular, renal diseases and in aging-associated conditions. Therefore, understanding of SIRT1-deficient, endothelial dysfunctional phenotype has much to offer clinically. Here, we summarize recent studies by several investigative teams of the characteristics of models of global endothelial SIRT1 deficiency, the causes of facilitative development of fibrosis in these conditions, dissect the protein composition of the aberrant secretome of SIRT1-deficient endothelial cells and present several components of this aberrant secretome that are involved in fibrogenesis via activation of fibroblasts to myofibroblasts. These include ligands of Wnt and Notch pathways, as well as proteolytic fragments of glycocalyx core protein, syndecan-4. The latter finding is crucial for understanding the degradation of glycocalyx that accompanies SIRT1 deficiency. This spectrum of abnormalities associated with SIRT1 deficiency in endothelial cells is essential for understanding the origins and features of endothelial dysfunction in a host of cardiovascular and renal diseases."],["dc.identifier.doi","10.3389/fphys.2018.01325"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15344"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59337"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.subject.ddc","610"],["dc.title","Fibrogenic Secretome of Sirtuin 1-Deficient Endothelial Cells: Wnt, Notch and Glycocalyx Rheostat"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","49"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association"],["dc.bibliographiccitation.lastpage","62"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Jeon, Noo Li"],["dc.contributor.author","Dadafarin, Sina"],["dc.contributor.author","Ratliff, Brian B."],["dc.contributor.author","Rowe, David W."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Goligorsky, Michael S."],["dc.date.accessioned","2019-08-07T07:45:39Z"],["dc.date.available","2019-08-07T07:45:39Z"],["dc.date.issued","2019"],["dc.description.abstract","Our laboratory has previously demonstrated that Sirt1endo-/- mice show endothelial dysfunction and exaggerated renal fibrosis, whereas mice with silenced endothelial transforming growth factor beta (TGF-β) signaling are resistant to fibrogenic signals. Considering the fact that the only difference between these mutant mice is confined to the vascular endothelium, this indicates that secreted substances contribute to these contrasting responses."],["dc.identifier.doi","10.1093/ndt/gfy100"],["dc.identifier.pmid","29726981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62334"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1460-2385"],["dc.relation.issn","0931-0509"],["dc.relation.issn","1460-2385"],["dc.title","Dickkopf-3 in aberrant endothelial secretome triggers renal fibroblast activation and endothelial-mesenchymal transition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","558"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","568"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Song, Jong W."],["dc.contributor.author","Matsumoto, Kei"],["dc.contributor.author","Dadafarin, Sina"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Müller, Gerhard"],["dc.contributor.author","Goligorsky, Michael S."],["dc.date.accessioned","2020-12-10T15:20:11Z"],["dc.date.available","2020-12-10T15:20:11Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.kint.2017.02.033"],["dc.identifier.issn","0085-2538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72580"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The third path of tubulointerstitial fibrosis: aberrant endothelial secretome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]