Lipphardt, Mark Frederik

[["dc.bibliographiccitation.firstpage","1287"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","1296"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Koziolek, Michael J."],["dc.contributor.author","Lehnig, Luca-Yves"],["dc.contributor.author","Schäfer, Ann-Kathrin"],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Lüders, Stephan"],["dc.contributor.author","Wallbach, Manuel"],["dc.date.accessioned","2020-12-10T14:10:22Z"],["dc.date.available","2020-12-10T14:10:22Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00392-019-01464-4"],["dc.identifier.eissn","1861-0692"],["dc.identifier.issn","1861-0684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70741"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Effect of baroreflex activation therapy on renal sodium excretion in patients with resistant hypertension"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3051"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Maas, Jens-Holger"],["dc.contributor.author","Schäfer, Ann-Kathrin"],["dc.contributor.author","Amlaz, Saskia I."],["dc.contributor.author","Ratliff, Brian B."],["dc.contributor.author","Koziolek, Michael J."],["dc.contributor.author","Wallbach, Manuel"],["dc.date.accessioned","2021-04-14T08:32:33Z"],["dc.date.available","2021-04-14T08:32:33Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/jcm9093051"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83944"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Syndecan-4 as a Marker of Endothelial Dysfunction in Patients with Resistant Hypertension"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","991"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Pflügers Archiv - European Journal of Physiology"],["dc.bibliographiccitation.lastpage","1002"],["dc.bibliographiccitation.volume","472"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Song, Jong Wook"],["dc.contributor.author","Goligorsky, Michael S"],["dc.date.accessioned","2021-04-14T08:26:09Z"],["dc.date.available","2021-04-14T08:26:09Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00424-020-02407-z"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81851"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-2013"],["dc.relation.issn","0031-6768"],["dc.title","Sirtuin 1 and endothelial glycocalyx"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","42"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","52"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Rudnicki, Michael"],["dc.contributor.author","Siwy, Justyna"],["dc.contributor.author","Wendt, Ralph"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Koziolek, Michael J"],["dc.contributor.author","Maixnerova, Dita"],["dc.contributor.author","Peters, Björn"],["dc.contributor.author","Kerschbaum, Julia"],["dc.contributor.author","Leierer, Johannes"],["dc.contributor.author","Neprasova, Michaela"],["dc.contributor.author","Peters, Björn"],["dc.contributor.authorgroup","PERSTIGAN working group"],["dc.date.accessioned","2022-02-01T10:31:22Z"],["dc.date.available","2022-02-01T10:31:22Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background Risk of kidney function decline in immunoglobulin A (IgA) nephropathy (IgAN) is significant and may not be predicted by available clinical and histological tools. To serve this unmet need, we aimed at developing a urinary biomarker-based algorithm that predicts rapid disease progression in IgAN, thus enabling a personalized risk stratification. Methods In this multicentre study, urine samples were collected in 209 patients with biopsy-proven IgAN. Progression was defined by tertiles of the annual change of estimated glomerular filtration rate (eGFR) during follow-up. Urine samples were analysed using capillary electrophoresis coupled mass spectrometry. The area under the receiver operating characteristic curve (AUC) was used to evaluate the risk prediction models. Results Of the 209 patients, 64% were male. Mean age was 42 years, mean eGFR was 63 mL/min/1.73 m2 and median proteinuria was 1.2 g/day. We identified 237 urine peptides showing significant difference in abundance according to the tertile of eGFR change. These included fragments of apolipoprotein C-III, alpha-1 antitrypsin, different collagens, fibrinogen alpha and beta, titin, haemoglobin subunits, sodium/potassium-transporting ATPase subunit gamma, uromodulin, mucin-2, fractalkine, polymeric Ig receptor and insulin. An algorithm based on these protein fragments (IgAN237) showed a significant added value for the prediction of IgAN progression [AUC 0.89; 95% confidence interval (CI) 0.83–0.95], as compared with the clinical parameters (age, gender, proteinuria, eGFR and mean arterial pressure) alone (0.72; 95% CI 0.64–0.81). Conclusions A urinary peptide classifier predicts progressive loss of kidney function in patients with IgAN significantly better than clinical parameters alone."],["dc.description.abstract","Abstract Background Risk of kidney function decline in immunoglobulin A (IgA) nephropathy (IgAN) is significant and may not be predicted by available clinical and histological tools. To serve this unmet need, we aimed at developing a urinary biomarker-based algorithm that predicts rapid disease progression in IgAN, thus enabling a personalized risk stratification. Methods In this multicentre study, urine samples were collected in 209 patients with biopsy-proven IgAN. Progression was defined by tertiles of the annual change of estimated glomerular filtration rate (eGFR) during follow-up. Urine samples were analysed using capillary electrophoresis coupled mass spectrometry. The area under the receiver operating characteristic curve (AUC) was used to evaluate the risk prediction models. Results Of the 209 patients, 64% were male. Mean age was 42 years, mean eGFR was 63 mL/min/1.73 m2 and median proteinuria was 1.2 g/day. We identified 237 urine peptides showing significant difference in abundance according to the tertile of eGFR change. These included fragments of apolipoprotein C-III, alpha-1 antitrypsin, different collagens, fibrinogen alpha and beta, titin, haemoglobin subunits, sodium/potassium-transporting ATPase subunit gamma, uromodulin, mucin-2, fractalkine, polymeric Ig receptor and insulin. An algorithm based on these protein fragments (IgAN237) showed a significant added value for the prediction of IgAN progression [AUC 0.89; 95% confidence interval (CI) 0.83–0.95], as compared with the clinical parameters (age, gender, proteinuria, eGFR and mean arterial pressure) alone (0.72; 95% CI 0.64–0.81). Conclusions A urinary peptide classifier predicts progressive loss of kidney function in patients with IgAN significantly better than clinical parameters alone."],["dc.identifier.doi","10.1093/ndt/gfaa307"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98841"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1460-2385"],["dc.relation.issn","0931-0509"],["dc.title","Urine proteomics for prediction of disease progression in patients with IgA nephropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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","1597"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Wallbach, Manuel"],["dc.contributor.author","Koziolek, Michael J."],["dc.date.accessioned","2021-04-14T08:26:23Z"],["dc.date.available","2021-04-14T08:26:23Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/jcm9051597"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81923"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Plasma Exchange or Immunoadsorption in Demyelinating Diseases: A Meta-Analysis"],["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","203"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","211"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Song, Jong Wook"],["dc.contributor.author","Zullo, Joseph"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Dragovich, Matthew"],["dc.contributor.author","Zhang, Frank X"],["dc.contributor.author","Fu, Bingmei"],["dc.contributor.author","Goligorsky, Michael S"],["dc.date.accessioned","2020-12-10T18:19:37Z"],["dc.date.available","2020-12-10T18:19:37Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/ndt/gfx076"],["dc.identifier.eissn","1460-2385"],["dc.identifier.issn","0931-0509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75310"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Endothelial glycocalyx—the battleground for complications of sepsis and kidney injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","992"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","STEM CELLS Translational Medicine"],["dc.bibliographiccitation.lastpage","1005"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Matsumoto, Kei"],["dc.contributor.author","Xavier, Sandhya"],["dc.contributor.author","Chen, Jun"],["dc.contributor.author","Kida, Yujiro"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Ikeda, Reina"],["dc.contributor.author","Gevertz, Annie"],["dc.contributor.author","Caviris, Mario"],["dc.contributor.author","Hatzopoulos, Antonis K."],["dc.contributor.author","Kalajzic, Ivo"],["dc.contributor.author","Dutton, James"],["dc.contributor.author","Ratliff, Brian B."],["dc.contributor.author","Zhao, Hong"],["dc.contributor.author","Darzynkiewicz, Zbygniew"],["dc.contributor.author","Rose-John, Stefan"],["dc.contributor.author","Goligorsky, Michael S."],["dc.date.accessioned","2019-03-04T11:18:43Z"],["dc.date.available","2019-03-04T11:18:43Z"],["dc.date.issued","2017"],["dc.description.abstract","Accumulation of myofibroblasts is a hallmark of renal fibrosis. A significant proportion of myofibroblasts has been reported to originate via endothelial-mesenchymal transition. We initially hypothesized that exposing myofibroblasts to the extract of endothelial progenitor cells (EPCs) could reverse this transition. Indeed, in vitro treatment of transforming growth factor-β1 (TGF-β1)-activated fibroblasts with EPC extract prevented expression of α-smooth muscle actin (α-SMA); however, it did not enhance expression of endothelial markers. In two distinct models of renal fibrosis-unilateral ureteral obstruction and chronic phase of folic acid-induced nephropathy-subcapsular injection of EPC extract to the kidney prevented and reversed accumulation of α-SMA-positive myofibroblasts and reduced fibrosis. Screening the composition of EPC extract for cytokines revealed that it is enriched in leukemia inhibitory factor (LIF) and vascular endothelial growth factor. Only LIF was capable of reducing fibroblast-to-myofibroblast transition of TGF-β1-activated fibroblasts. In vivo subcapsular administration of LIF reduced the number of myofibroblasts and improved the density of peritubular capillaries; however, it did not reduce the degree of fibrosis. A receptor-independent ligand for the gp130/STAT3 pathway, hyper-interleukin-6 (hyper-IL-6), not only induced a robust downstream increase in pluripotency factors Nanog and c-Myc but also exhibited a powerful antifibrotic effect. In conclusion, EPC extract prevented and reversed fibroblast-to-myofibroblast transition and renal fibrosis. The component of EPC extract, LIF, was capable of preventing development of the contractile phenotype of activated fibroblasts but did not eliminate TGF-β1-induced collagen synthesis in cultured fibroblasts and models of renal fibrosis, whereas a receptor-independent gp130/STAT3 agonist, hyper-IL-6, prevented fibrosis. In summary, these studies, through the evolution from EPC extract to LIF and then to hyper-IL-6, demonstrate the instructive role of microenvironmental cues and may provide in the future a facile strategy to prevent and reverse renal fibrosis. Stem Cells Translational Medicine 2017;6:992-1005."],["dc.identifier.doi","10.5966/sctm.2016-0095"],["dc.identifier.pmid","28297566"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57662"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Instructive Role of the Microenvironment in Preventing Renal Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","421"],["dc.bibliographiccitation.journal","Matrix Biology"],["dc.bibliographiccitation.lastpage","431"],["dc.bibliographiccitation.volume","71-72"],["dc.contributor.author","Zhang, Xiaohui"],["dc.contributor.author","Sun, Dong"],["dc.contributor.author","Song, Jeon W."],["dc.contributor.author","Zullo, Joseph"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Coneh-Gould, Leona"],["dc.contributor.author","Goligorsky, Michael S."],["dc.date.accessioned","2020-12-10T15:20:19Z"],["dc.date.available","2020-12-10T15:20:19Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.matbio.2018.01.026"],["dc.identifier.issn","0945-053X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72624"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Endothelial cell dysfunction and glycocalyx – A vicious circle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]