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Book ; Thesis: Studien zur Rolle von Wachstumsfaktoren/Zytokinen und therapeutischen Interventionsstrategien in der mesangioproliferativen Glomerulonephritis

Ostendorf, Tammo

2002

Author's details	vorgelegt von Tammo Ostendorf
Language	German
Size	132 S. : Ill., graph. Darst.
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Aachen, Techn. Hochsch., Habil.-Schr., 2002
HBZ-ID	HT013677425
Database	Catalogue ZB MED Medicine, Health

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2004 E 19	order to use in reading room	Magazin

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Article ; Online: Key metalloproteinase-mediated pathways in the kidney.

Wozniak, Justyna / Floege, Jürgen / Ostendorf, Tammo / Ludwig, Andreas

Nature reviews. Nephrology

2021 Volume 17, Issue 8, Page(s) 513–527

Abstract: Matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinases (ADAMs) belong to the metzincin family of zinc-containing multidomain molecules, and can act as soluble or membrane-bound proteases. These enzymes inactivate or activate other ... ...

Abstract	Matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinases (ADAMs) belong to the metzincin family of zinc-containing multidomain molecules, and can act as soluble or membrane-bound proteases. These enzymes inactivate or activate other soluble or membrane-expressed mediator molecules, which enables them to control developmental processes, tissue remodelling, inflammatory responses and proliferative signalling pathways. The dysregulation of MMPs and ADAMs has long been recognized in acute kidney injury and in chronic kidney disease, and genetic targeting of selected MMPs and ADAMs in different mouse models of kidney disease showed that they can have detrimental and protective roles. In particular, MMP-2, MMP-7, MMP-9, ADAM10 and ADAM17 have been shown to have a mainly profibrotic effect and might therefore represent therapeutic targets. Each of these proteases has been associated with a different profibrotic pathway that involves tissue remodelling, Wnt-β-catenin signalling, stem cell factor-c-kit signalling, IL-6 trans-signalling or epidermal growth factor receptor (EGFR) signalling. Broad-spectrum metalloproteinase inhibitors have been used to treat fibrotic kidney diseases experimentally but more targeted approaches have since been developed, including inhibitory antibodies, to avoid the toxic side effects initially observed with broad-spectrum inhibitors. These advances not only provide a solid foundation for additional preclinical studies but also encourage further translation into clinical research.
MeSH term(s)	ADAM Proteins/metabolism ; Animals ; Humans ; Kidney/metabolism ; Kidney Diseases/metabolism ; Matrix Metalloproteinases/metabolism ; Metabolic Networks and Pathways ; Metalloproteases/metabolism
Chemical Substances	Metalloproteases (EC 3.4.-) ; ADAM Proteins (EC 3.4.24.-) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2021-04-20
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-021-00415-5
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Zs.A 6334: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 107: Show issues

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Article ; Online: Lineage tracing reveals transient phenotypic adaptation of tubular cells during acute kidney injury.

Buse, Marc / Cheng, Mingbo / Jankowski, Vera / Lellig, Michaela / Sterzer, Viktor / Strieder, Thiago / Leuchtle, Katja / Martin, Ina V / Seikrit, Claudia / Brinkkoettter, Paul / Crispatzu, Giuliano / Floege, Jürgen / Boor, Peter / Speer, Timotheus / Kramann, Rafael / Ostendorf, Tammo / Moeller, Marcus J / Costa, Ivan G / Stamellou, Eleni

iScience

2024 Volume 27, Issue 3, Page(s) 109255

Abstract: Tubular injury is the hallmark of acute kidney injury (AKI) with a tremendous impact on patients and health-care systems. During injury, any differentiated proximal tubular cell (PT) may transition into a specific injured phenotype, so-called "scattered ... ...

Abstract	Tubular injury is the hallmark of acute kidney injury (AKI) with a tremendous impact on patients and health-care systems. During injury, any differentiated proximal tubular cell (PT) may transition into a specific injured phenotype, so-called "scattered tubular cell" (STC)-phenotype. To understand the fate of this specific phenotype, we generated transgenic mice allowing inducible, reversible, and irreversible tagging of these cells in a murine AKI model, the unilateral ischemia-reperfusion injury (IRI). For lineage tracing, we analyzed the kidneys using single-cell profiling during disease development at various time points. Labeled cells, which we defined by established endogenous markers, already appeared 8 h after injury and showed a distinct expression set of genes. We show that STCs re-differentiate back into fully differentiated PTs upon the resolution of the injury. In summary, we show the dynamics of the phenotypic transition of PTs during injury, revealing a reversible transcriptional program as an adaptive response during disease.
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109255
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Article ; Online: DNA binding protein YB-1 is a part of the neutrophil extracellular trap mediation of kidney damage and cross-organ effects.

Wang, Jialin / Liu, Xiyang / Gu, Yulu / Gao, Yingying / Jankowski, Vera / Was, Nina / Leitz, Anna / Reiss, Lucy K / Shi, Yiqin / Cai, Jieru / Fang, Yi / Song, Nana / Zhao, Shuan / Floege, Jürgen / Ostendorf, Tammo / Ding, Xiaoqiang / Raffetseder, Ute

Kidney international

2023 Volume 104, Issue 1, Page(s) 124–138

Abstract: Open-heart surgery is associated with high morbidity, with acute kidney injury (AKI) being one of the most commonly observed postoperative complications. Following open-heart surgery, in an observational study we found significantly higher numbers of ... ...

Abstract	Open-heart surgery is associated with high morbidity, with acute kidney injury (AKI) being one of the most commonly observed postoperative complications. Following open-heart surgery, in an observational study we found significantly higher numbers of blood neutrophils in a group of 13 patients with AKI compared to 25 patients without AKI (AKI: 12.9±5.4 ×10
MeSH term(s)	Mice ; Animals ; Extracellular Traps ; DNA-Binding Proteins ; Lipopolysaccharides ; Kidney ; Acute Kidney Injury ; Ischemia/complications ; Hypoxia ; Immunoglobulin G ; Reperfusion Injury/complications ; Mice, Inbred C57BL
Chemical Substances	DNA-Binding Proteins ; Lipopolysaccharides ; Immunoglobulin G
Language	English
Publishing date	2023-03-22
Publishing country	United States
Document type	Observational Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.02.032
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Article ; Online: Inhibition of the glucocorticoid receptor attenuates proteinuric kidney diseases in multiple species.

Stamellou, Eleni / Agrawal, Shipra / Siegerist, Florian / Buse, Marc / Kuppe, Christoph / Lange, Tim / Buhl, Eva Miriam / Alam, Jessica / Strieder, Thiago / Boor, Peter / Ostendorf, Tammo / Gröne, Hermann-Josef / Floege, Jürgen / Smoyer, William E / Endlich, Nicole / Moeller, Marcus J

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2023

Abstract: Background and hypothesis: Glucocorticoids are the treatment of choice for proteinuric patients with minimal-change disease (MCD) and primary focal and segmental glomerulosclerosis (FSGS). Immunosuppressive as well as direct effects on podocytes are ... ...

Abstract	Background and hypothesis: Glucocorticoids are the treatment of choice for proteinuric patients with minimal-change disease (MCD) and primary focal and segmental glomerulosclerosis (FSGS). Immunosuppressive as well as direct effects on podocytes are believed to mediate their actions. In this study, we analyzed the anti-proteinuric effects of inhibition of the glucocorticoid receptor (GR) in glomerular epithelial cells, including podocytes. Methods: We employed genetic and pharmacological approaches to inhibit the GR. Genetically, we used Pax8-Cre/GRfl/fl mice to specifically inactivate the GR in kidney epithelial cells. Pharmacologically, we utilized a glucocorticoid antagonist called mifepristone. Results: Genetic inactivation of GR, specifically in kidney epithelial cells, using Pax8-Cre/GRfl/fl mice, ameliorated proteinuria following protein overload. We further tested the effects of pharmacological GR inhibition in three models and species: the puromycin-aminonucleoside-induced nephrosis model in rats, the protein overload model in mice and the inducible transgenic NTR/MTZ zebrafish larvae with specific and reversible podocyte injury. In all three models, both pharmacological GR activation and inhibition consistently and significantly ameliorated proteinuria. Additionally, we translated our findings to humans, where three nephrotic adult patients with MCD or primary FSGS with contraindications or insufficient responses to corticosteroids, were treated with mifepristone. This treatment resulted in a clinically relevant reduction of proteinuria. Conclusions: Thus, across multiple species and proteinuria models, both genetic and pharmacological GR inhibition was at least as effective as pronounced GR activation. While, the mechanism remains perplexing, GR inhibition may be a novel and targeted therapeutic approach to treat glomerular proteinuria potentially bypassing adverse actions of steroids.
Language	English
Publishing date	2023-11-30
Publishing country	England
Document type	Journal Article
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfad254
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 329: Show issues

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Article: New Aspects of Kidney Fibrosis-From Mechanisms of Injury to Modulation of Disease.

Moeller, Marcus J / Kramann, Rafael / Lammers, Twan / Hoppe, Bernd / Latz, Eicke / Ludwig-Portugall, Isis / Boor, Peter / Floege, Jürgen / Kurts, Christian / Weiskirchen, Ralf / Ostendorf, Tammo

Frontiers in medicine

2022 Volume 8, Page(s) 814497

Abstract: Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative ... ...

Abstract	Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative Research Center "Organ Fibrosis: From Mechanisms of Injury to Modulation of Disease" (referred to as SFB/TRR57) was hosted from 2009 to 2021 by the Medical Faculties of RWTH Aachen University and the University of Bonn. This consortium had the ultimate goal of discovering new common but also different fibrosis pathways in the liver and kidneys. It finally successfully identified new mechanisms and established novel therapeutic approaches to interfere with hepatic and renal fibrosis. This review covers the consortium's key kidney-related findings, where three overarching questions were addressed: (i) What are new relevant mechanisms and signaling pathways triggering renal fibrosis? (ii) What are new immunological mechanisms, cells and molecules that contribute to renal fibrosis?, and finally (iii) How can renal fibrosis be modulated?
Language	English
Publishing date	2022-01-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2021.814497
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Article ; Online: New Aspects of Kidney Fibrosis–From Mechanisms of Injury to Modulation of Disease

Marcus J. Moeller / Rafael Kramann / Twan Lammers / Bernd Hoppe / Eicke Latz / Isis Ludwig-Portugall / Peter Boor / Jürgen Floege / Christian Kurts / Ralf Weiskirchen / Tammo Ostendorf

Frontiers in Medicine, Vol

2022 Volume 8

Abstract	Organ fibrogenesis is characterized by a common pathophysiological final pathway independent of the underlying progressive disease of the respective organ. This makes it particularly suitable as a therapeutic target. The Transregional Collaborative Research Center “Organ Fibrosis: From Mechanisms of Injury to Modulation of Disease” (referred to as SFB/TRR57) was hosted from 2009 to 2021 by the Medical Faculties of RWTH Aachen University and the University of Bonn. This consortium had the ultimate goal of discovering new common but also different fibrosis pathways in the liver and kidneys. It finally successfully identified new mechanisms and established novel therapeutic approaches to interfere with hepatic and renal fibrosis. This review covers the consortium's key kidney-related findings, where three overarching questions were addressed: (i) What are new relevant mechanisms and signaling pathways triggering renal fibrosis? (ii) What are new immunological mechanisms, cells and molecules that contribute to renal fibrosis?, and finally (iii) How can renal fibrosis be modulated?
Keywords	renal fibrosis ; myofibroblast ; parietal epithelial cell ; inflammasome ; crystals ; lupus erythematodes ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: PDGF and the progression of renal disease.

Boor, Peter / Ostendorf, Tammo / Floege, Jürgen

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2014 Volume 29 Suppl 1, Page(s) i45–i54

Abstract: Progressive renal diseases represent a global medical problem, in part because we currently lack effective treatment strategies. Inhibition of platelet-derived growth factors (PDGFs) might represent one such novel strategy. PDGFs are required for normal ... ...

Abstract	Progressive renal diseases represent a global medical problem, in part because we currently lack effective treatment strategies. Inhibition of platelet-derived growth factors (PDGFs) might represent one such novel strategy. PDGFs are required for normal kidney development by the recruitment of mesenchymal cells to both glomeruli and the interstitium. PDGFs are expressed in renal mesenchymal cells and, upon injury, in epithelial and infiltrating cells. They exert autocrine and paracrine effects on PDGF receptor-bearing mesenchymal cells, i.e. mesangial cells, fibroblasts and vascular smooth-muscle cells, which are crucially involved in progressive renal diseases. Proliferation but also migration and activation of these mesenchymal cells are the major effects mediated by PDGFs. These actions predefine the major roles of PDGFs in renal pathology, particularly in mesangioproliferative glomerulonephritis and interstitial fibrosis. Whereas for the former, the role of PDGFs is very well described and established, the latter is increasingly better documented as well. An involvement of PDGFs in other renal diseases, e.g. acute kidney injury, vascular injury and hypertensive as well as diabetic nephropathy, is less well established or presently unknown. Nevertheless, PDGFs represent a promising therapeutic option for progressive renal diseases, especially those characterized by mesangial cell proliferation and interstitial fibrosis. Clinical studies are eagerly awaited, in particular, since several drugs inhibiting PDGF signalling are available for clinical testing.
MeSH term(s)	Animals ; Disease Progression ; Humans ; Kidney Diseases/diagnosis ; Kidney Diseases/metabolism ; Platelet-Derived Growth Factor/metabolism
Chemical Substances	Platelet-Derived Growth Factor
Language	English
Publishing date	2014-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gft273
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 329: Show issues

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Article: Platelet-derived growth factors (PDGFs) in glomerular and tubulointerstitial fibrosis.

Ostendorf, Tammo / Boor, Peter / van Roeyen, Claudia R C / Floege, Jürgen

Kidney international supplements

2015 Volume 4, Issue 1, Page(s) 65–69

Abstract: Renal fibrosis is the hallmark of chronic kidney disease progression and is characterized by an exaggerated wound-healing process with the production of renal scar tissue. It comprises both the glomerular and the tubulointerstitial compartments. Among ... ...

Abstract	Renal fibrosis is the hallmark of chronic kidney disease progression and is characterized by an exaggerated wound-healing process with the production of renal scar tissue. It comprises both the glomerular and the tubulointerstitial compartments. Among the factors that contribute to kidney fibrosis, the members of the platelet-derived growth factor (PDGF) family are among the best characterized ones. They appear to be the key factors in driving renal fibrosis, independent of the underlying kidney disease. The PDGF family consists of four isoforms (PDGF-A, -B, -C, and -D) and two receptor chains (PDGFR-α and -β), which are constitutively or inducibly expressed in most renal cells. These components have an irreplaceable role in kidney development by recruitment of mesenchymal cells to the glomerular and tubulointerstitial compartments. They further regulate multiple pathophysiologic processes including cell proliferation, cell migration, expression and accumulation of extracellular matrix, production and secretion of pro- and anti-inflammatory mediators, vascular permeability, and hemodynamics. This review provides a brief update on the role of different PDGF isoforms in the development of glomerulosclerosis and tubulointerstitial fibrosis, newly identified endogeneous PDGF antagonists, and resulting potential therapies.
Language	English
Publishing date	2015-07-31
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	193442-9
ISSN	2157-1716 ; 2157-1724 ; 0098-6577
ISSN (online)	2157-1716
ISSN	2157-1724 ; 0098-6577
DOI	10.1038/kisup.2014.12
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Zs.A 797 -Suppl.-: Show issues

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Article: High-fat diet-induced obesity causes an inflammatory microenvironment in the kidneys of aging Long-Evans rats.

Laurentius, Thea / Raffetseder, Ute / Fellner, Claudia / Kob, Robert / Nourbakhsh, Mahtab / Floege, Jürgen / Bertsch, Thomas / Bollheimer, Leo Cornelius / Ostendorf, Tammo

Journal of inflammation (London, England)

2019 Volume 16, Page(s) 14

Abstract: Background: Obesity is a risk factor for chronic kidney disease (CKD). While the exact mechanisms remain unclear, inflammation may be a consequence of obesity that directly impacts the kidneys. The aim of this study was to examine the inflammatory ... ...

Abstract	Background: Obesity is a risk factor for chronic kidney disease (CKD). While the exact mechanisms remain unclear, inflammation may be a consequence of obesity that directly impacts the kidneys. The aim of this study was to examine the inflammatory status of the kidneys and potential ongoing renal damage, i.e., tubular damage and fibrosis after long-term obesity maintained through persistent consumption of a high-fat diet (HFD). Results: Twenty-four-week-old male Long-Evans (LEV) rats were continuously fed a control diet (CD) or HFD for 51 weeks. The mean body weight was higher in HFD-fed rats than in control diet-fed rats and markedly elevated during the last 24 weeks. Blood analyses revealed no substantial alterations in renal functional parameters by HFD consumption but a substantial increase in creatine kinase, a muscle loss marker. Magnetic resonance imaging (MRI) was utilized to quantify rat quadriceps muscle mass. The data showed that HFD-induced obesity in LEV rats was accompanied by minor decreases in muscle mass and strength at 75 weeks of age. Rat kidney inflammatory status was evaluated using histological and immunohistological techniques. The number of foci with immune cell infiltrates and infiltrating monocytes/macrophages was significantly increased in HFD-fed rat kidneys at week 75. Renal fibrosis parameters, including glomerulosclerosis and tubular damage, were also markedly increased in renal tissues from HFD-fed rats compared to the controls. The significant increase in tubular protein casts in HFD-fed rat tissues indicated that renal function was already disturbed. Rat kidney inflammatory status was further evaluated using the simultaneous profiling of twenty-two inflammatory markers in kidney tissue extracts. Consistently, MCP-1 and eotaxin (CCL11) levels were elevated in obese LEV rat kidneys. Conclusions: Compared to CD-fed rats, HFD-fed obese LEV rats show significant damage of renal structures with aging. These subtle changes may sensitize the kidneys to the development of progressive CKD.
Language	English
Publishing date	2019-06-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2164385-4
ISSN	1476-9255
ISSN	1476-9255
DOI	10.1186/s12950-019-0219-x
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