Korsten, Peter

[["dc.bibliographiccitation.artnumber","208"],["dc.bibliographiccitation.journal","Frontiers in Medicine"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Rademacher, Jan-Gerd"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2019-09-24T08:03:09Z"],["dc.date.available","2019-09-24T08:03:09Z"],["dc.date.issued","2019"],["dc.description.abstract","Raynaud's phenomenon (RP) is almost universally present in patients with Systemic Sclerosis (SSc). RP represents a generalized vasculopathy and potentially lead to digital ulcers (DU), which may be complicated by superinfection, tissue necrosis, and limb loss. We report the analysis of an extracorporeal procedure in a 36-year-old female patient with diffuse SSc with refractory RP and DU despite treatment with diltiazem, candesartan, sildenafil, and intravenous iloprost. We performed rheopheresis (RheoP), a variant of double-filtration plasmapheresis, as a potential new treatment option for refractory patients despite optimal medical therapy. We performed two RheoP per week every 4 weeks for a total of 3 months. Clinical improvement in DU healing occurred with no adverse events directly related to the treatment. While there was no reduction in the number of Raynaud attacks with RheoP, a significant reduction of the duration of attacks from a median of 15 (5–45, 95% CI 10–15) to 7 (3–30, 95% CI 6–10) minutes with an improvement of the Raynaud Condition Score (RCS) improved from 4 to 2. In conclusion, RheoP is a feasible and potentially beneficial treatment modality in patients with refractory RP and DU. We propose that RheoP should be investigated in a larger number of patients in a clinical trial setting."],["dc.identifier.doi","10.3389/fmed.2019.00208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62449"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2296-858X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Rheopheresis for Digital Ulcers and Raynaud's Phenomenon in Systemic Sclerosis Refractory to Conventional Treatments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2072143"],["dc.bibliographiccitation.journal","Human Vaccines & Immunotherapeutics"],["dc.contributor.author","Plüß, Marlene"],["dc.contributor.author","Piantoni, Silvia"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Kim, Alfred H. J."],["dc.contributor.author","Korsten, Peter"],["dc.date.accessioned","2022-06-01T09:39:18Z"],["dc.date.available","2022-06-01T09:39:18Z"],["dc.date.issued","2022"],["dc.description.abstract","In recent years, advances in the treatment and management of patients with systemic lupus erythematosus (SLE) have improved their life expectancy and quality of life. However, lupus nephritis (LN) still represents a major life-threatening complication of the disease. Belimumab (BEL), a fully human monoclonal IgG1λ antibody neutralizing soluble B cell activating factor, was approved more than ten years ago as add-on therapy in adults and pediatric patients with a highly active, autoantibody-positive disease despite standard of care (SoC). Recently, the superiority of the addition of BEL to SoC was also demonstrated in LN. In this review, we provide a comprehensive overview of the study landscape, available therapeutic options for SLE (focusing on BEL in renal and non-renal SLE), and new perspectives in the treatment field of this disease. A personalized treatment approach will likely become available with the advent of novel therapeutic agents for SLE and LN."],["dc.identifier.doi","10.1080/21645515.2022.2072143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108436"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2164-554X"],["dc.relation.issn","2164-5515"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Belimumab for systemic lupus erythematosus – Focus on lupus nephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2682"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-08-12T07:45:59Z"],["dc.date.available","2021-08-12T07:45:59Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA). Acute tubular injury with the presence of tubulitis was previously reported to be of prognostic value in ANCA glomerulonephritis (GN). In particular, distinct tubular injury lesions were associated with the deterioration of kidney function at AAV disease onset, as well as renal resistance to treatment, and higher risk of progression to composite outcome in patients with AAV. To expand our knowledge regarding distinct tubular lesions in AAV, we aimed to describe acute tubular injury patterns in association with glomerular lesions in ANCA GN by systematic histological scoring. Methods: A total number of 48 renal biopsies with confirmed renal involvement of AAV admitted to the University Medical Center Göttingen from 2015 to 2020 were retrospectively examined. By systematic scoring of tubular injury lesions, the association between clinical parameters, laboratory markers, and histopathological findings was explored. Results: We have shown that cellular casts in renal biopsies were frequently observed in the majority of cases with ANCA GN. Furthermore, we showed that tubular epithelial simplification with dilatation correlated with MPA and MPO subtypes, C3c hypocomplementemia, severe renal involvement, and uACR. Red blood cell (RBC) casts were associated with increased levels of C-reactive protein (CRP), leukocyturia, and hematuria. Finally, we found that hyaline casts were associated with an increased fraction of glomeruli with global glomerular sclerosis. Conclusions: Acute tubular injury patterns were correlated with active ANCA GN, whereas tubular injury lesions reflecting the later stages of kidney disease correlated with chronic glomerular lesions. These results suggest an interplay between different renal compartments."],["dc.description.abstract","Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA). Acute tubular injury with the presence of tubulitis was previously reported to be of prognostic value in ANCA glomerulonephritis (GN). In particular, distinct tubular injury lesions were associated with the deterioration of kidney function at AAV disease onset, as well as renal resistance to treatment, and higher risk of progression to composite outcome in patients with AAV. To expand our knowledge regarding distinct tubular lesions in AAV, we aimed to describe acute tubular injury patterns in association with glomerular lesions in ANCA GN by systematic histological scoring. Methods: A total number of 48 renal biopsies with confirmed renal involvement of AAV admitted to the University Medical Center Göttingen from 2015 to 2020 were retrospectively examined. By systematic scoring of tubular injury lesions, the association between clinical parameters, laboratory markers, and histopathological findings was explored. Results: We have shown that cellular casts in renal biopsies were frequently observed in the majority of cases with ANCA GN. Furthermore, we showed that tubular epithelial simplification with dilatation correlated with MPA and MPO subtypes, C3c hypocomplementemia, severe renal involvement, and uACR. Red blood cell (RBC) casts were associated with increased levels of C-reactive protein (CRP), leukocyturia, and hematuria. Finally, we found that hyaline casts were associated with an increased fraction of glomeruli with global glomerular sclerosis. Conclusions: Acute tubular injury patterns were correlated with active ANCA GN, whereas tubular injury lesions reflecting the later stages of kidney disease correlated with chronic glomerular lesions. These results suggest an interplay between different renal compartments."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/jcm10122682"],["dc.identifier.pii","jcm10122682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88590"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Systematic Scoring of Tubular Injury Patterns Reveals Interplay between Distinct Tubular and Glomerular Lesions in ANCA-Associated Glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","annrheumdis-2020-218491"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Larsen, Jörg"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1136/annrheumdis-2020-218491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85655"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Repeated false-negative tests delayed diagnosis of COVID-19 in a case with granulomatosis with polyangiitis under maintenance therapy with rituximab and concomitant influenza pneumonia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-05-02T08:09:46Z"],["dc.date.available","2022-05-02T08:09:46Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s40620-022-01320-1"],["dc.identifier.pii","1320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107458"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1724-6059"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","pANCA autoantibody testing by indirect immunofluorescence indicates interstitial arteritis independent of MPO-ANCA immunoassays in ANCA-associated glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2014"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Schridde, Laura"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-10-01T09:58:23Z"],["dc.date.available","2021-10-01T09:58:23Z"],["dc.date.issued","2021"],["dc.description.abstract","Kidney fibrosis is a common manifestation and hallmark of a wide variety of chronic kidney disease (CKD) that appears in different morphological patterns, suggesting distinct pathogenic causes. Broad macroscopically visible scars are the sequelae of severe focal injury and complete parenchymal destruction, reflecting a wound healing response as a consequence of infarction. In the kidney, chronic glomerular injury leads to atrophy of the corresponding tubule, degeneration of this specific nephron, and finally interstitial fibrosis/tubular atrophy (IF/TA). Compared to this glomerulus-induced focal replacement scar, diffuse fibrosis independent of tubular atrophy appears to be a different pathogenic process. Kidney fibrosis appears to develop in a compartment-specific manner, but whether focal and diffuse fibrosis has distinct characteristics associated with other glomerular or tubulointerstitial lesions remains elusive. In the present study, we aimed to analyze renal fibrotic patterns related to renal lesions, which directly contribute to renal fibrogenesis, to unravel fibrotic patterns and manifestations upon damage to distinct renal compartments. Patterns of kidney fibrosis were analyzed in experimental models of CKD and various renal pathologies in correlation with histopathological and ultrastructural findings. After the induction of isolated crescentic glomerulonephritis (GN) in nephrotoxic serum-nephritis (NTN), chronic glomerular damage resulted in predominantly focal fibrosis adjacent to atrophic tubules. By contrast, using unilateral ureteral obstruction (UUO) as a model of primary injury to the tubulointerstitial compartment revealed diffuse fibrosis as the predominant pattern of chronic lesions. Finally, folic acid-induced nephropathy (FAN) as a model of primary tubular injury with consecutive tubular atrophy independent of chronic glomerular damage equally induced predominant focal IF/TA. By analyzing several renal pathologies, our data also suggest that focal and diffuse fibrosis appear to contribute as chronic lesions in the majority of human renal disease, mainly being present in antineutrophil cytoplasmic antibody (ANCA)-associated GN, lupus nephritis, and IgA nephropathy (IgAN). Focal IF/TA correlated with glomerular damage and irreversible injury to nephrons, whereas diffuse fibrosis in ANCA GN was associated explicitly with interstitial inflammation independent of glomerular damage and nephron loss. Ultrastructural analysis of focal IF/TA versus diffuse fibrosis revealed distinct matrix compositions, further supported by different collagen signatures in transcriptome datasets. With regard to long-term renal outcome, only the extent of focal IF/TA correlated with the development of end-stage kidney disease (ESKD) in ANCA GN. In contrast, diffuse kidney fibrosis did not associate with the long-term renal outcome. In conclusion, we here provide evidence that a focal pattern of kidney fibrosis seems to be associated with nephron loss and replacement scarring. In contrast, a diffuse pattern of kidney fibrosis appears to result from primary interstitial inflammation and injury."],["dc.description.abstract","Kidney fibrosis is a common manifestation and hallmark of a wide variety of chronic kidney disease (CKD) that appears in different morphological patterns, suggesting distinct pathogenic causes. Broad macroscopically visible scars are the sequelae of severe focal injury and complete parenchymal destruction, reflecting a wound healing response as a consequence of infarction. In the kidney, chronic glomerular injury leads to atrophy of the corresponding tubule, degeneration of this specific nephron, and finally interstitial fibrosis/tubular atrophy (IF/TA). Compared to this glomerulus-induced focal replacement scar, diffuse fibrosis independent of tubular atrophy appears to be a different pathogenic process. Kidney fibrosis appears to develop in a compartment-specific manner, but whether focal and diffuse fibrosis has distinct characteristics associated with other glomerular or tubulointerstitial lesions remains elusive. In the present study, we aimed to analyze renal fibrotic patterns related to renal lesions, which directly contribute to renal fibrogenesis, to unravel fibrotic patterns and manifestations upon damage to distinct renal compartments. Patterns of kidney fibrosis were analyzed in experimental models of CKD and various renal pathologies in correlation with histopathological and ultrastructural findings. After the induction of isolated crescentic glomerulonephritis (GN) in nephrotoxic serum-nephritis (NTN), chronic glomerular damage resulted in predominantly focal fibrosis adjacent to atrophic tubules. By contrast, using unilateral ureteral obstruction (UUO) as a model of primary injury to the tubulointerstitial compartment revealed diffuse fibrosis as the predominant pattern of chronic lesions. Finally, folic acid-induced nephropathy (FAN) as a model of primary tubular injury with consecutive tubular atrophy independent of chronic glomerular damage equally induced predominant focal IF/TA. By analyzing several renal pathologies, our data also suggest that focal and diffuse fibrosis appear to contribute as chronic lesions in the majority of human renal disease, mainly being present in antineutrophil cytoplasmic antibody (ANCA)-associated GN, lupus nephritis, and IgA nephropathy (IgAN). Focal IF/TA correlated with glomerular damage and irreversible injury to nephrons, whereas diffuse fibrosis in ANCA GN was associated explicitly with interstitial inflammation independent of glomerular damage and nephron loss. Ultrastructural analysis of focal IF/TA versus diffuse fibrosis revealed distinct matrix compositions, further supported by different collagen signatures in transcriptome datasets. With regard to long-term renal outcome, only the extent of focal IF/TA correlated with the development of end-stage kidney disease (ESKD) in ANCA GN. In contrast, diffuse kidney fibrosis did not associate with the long-term renal outcome. In conclusion, we here provide evidence that a focal pattern of kidney fibrosis seems to be associated with nephron loss and replacement scarring. In contrast, a diffuse pattern of kidney fibrosis appears to result from primary interstitial inflammation and injury."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/cells10082014"],["dc.identifier.pii","cells10082014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90053"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Different Patterns of Kidney Fibrosis Are Indicative of Injury to Distinct Renal Compartments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","annrheumdis-2020-218836"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1136/annrheumdis-2020-218836"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85656"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Correspondence on ‘Interleukin-6 receptor blockade with subcutaneous tocilizumab in severe COVID-19 pneumonia and hyperinflammation: case–control study’"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1231"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T09:42:37Z"],["dc.date.available","2021-06-01T09:42:37Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic vasculitis, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA). Kidney involvement is a common and severe complication of ANCA AAV which is observed in a considerable subset of patients, mainly affecting glomeruli. However, tubulointerstitial lesions have also been described in ANCA glomerulonephritis (GN). Therefore, we aim to describe active and chronic tubulointerstitial lesions in ANCA GN subtypes by systematic scoring analogous to the Banff scoring system while also utilizing clinical and laboratory findings. Methods: A total of 49 kidney biopsies with ANCA GN were retrospectively included in a single-center cohort study between 2015–2020. Results: We report that MPO-ANCA GN is associated with more severe deterioration of kidney function independent of systemic markers of AAV disease activity, and is also associated with increased proteinuria in MPO-ANCA GN and a decreased fraction of normal glomeruli. Finally, MPO-ANCA GN showed distinct, active, and chronic tubulointerstitial lesions. Conclusion: New insights into the pathophysiology of both entities, as well as differences in the clinical presentation of MPO- versus PR3-ANCA GN, could potentially pave the way for more precise treatment regimens. Therefore, it is important to understand the differences in histopathological presentation, especially in yet underestimated active tubulointerstitial lesions of ANCA GN subtypes. This research could further improve our understanding of distinct pathophysiological mechanisms."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.identifier.doi","10.3390/jcm10061231"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85302"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Systematic Histological Scoring Reveals More Prominent Interstitial Inflammation in Myeloperoxidase-ANCA Compared to Proteinase 3-ANCA Glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Steinle, Ulrike"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Carstens, Julienne L."],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2020-05-04T07:22:12Z"],["dc.date.available","2020-05-04T07:22:12Z"],["dc.date.issued","2017"],["dc.description.abstract","Acute kidney injury (AKI) and progressive chronic kidney disease (CKD) are intrinsically tied syndromes. In this regard, the acutely injured kidney often does not achieve its full regenerative capacity and AKI directly transitions into progressive CKD associated with tubulointerstitial fibrosis. Underlying mechanisms of such AKI-to-CKD progression are still incompletely understood and specific therapeutic interventions are still elusive. Because epigenetic modifications play a role in maintaining tissue fibrosis, we used a murine model of ischemia-reperfusion injury to determine whether aberrant promoter methylation of RASAL1 contributes causally to the switch between physiological regeneration and tubulointerstitial fibrogenesis, a hallmark of AKI-to-CKD progression. It is known that the antihypertensive drug hydralazine has demethylating activity, and that its optimum demethylating activity occurs at concentrations below blood pressure-lowering doses. Administration of low-dose hydralazine effectively induced expression of hydroxylase TET3, which catalyzed RASAL1 hydroxymethylation and subsequent RASAL1 promoter demethylation. Hydralazine-induced CpG promoter demethylation subsequently attenuated renal fibrosis and preserved excretory renal function independent of its blood pressure-lowering effects. In comparison, RASAL1 demethylation and inhibition of tubulointerstitial fibrosis was not detected upon administration of the angiotensin-converting enzyme inhibitor Ramipril in this model. Thus, RASAL1 promoter methylation and subsequent transcriptional RASAL1 suppression plays a causal role in AKI-to-CKD progression."],["dc.identifier.doi","10.1016/j.kint.2016.07.042"],["dc.identifier.pmid","27692563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64543"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/307"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | D03: ENPP3-vermittelter Phosphat-Metabolismus bei der Herzfibrose"],["dc.relation.eissn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Low-dose hydralazine prevents fibrosis in a murine model of acute kidney injury-to-chronic kidney disease progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","159"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Scleroderma and Related Disorders"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Rademacher, Jan-Gerd"],["dc.contributor.author","Wincup, Chris"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Korsten, Peter"],["dc.date.accessioned","2020-12-10T18:38:40Z"],["dc.date.available","2020-12-10T18:38:40Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1177/2397198319876738"],["dc.identifier.eissn","2397-1991"],["dc.identifier.issn","2397-1983"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77408"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Combination therapy with bosentan and sildenafil for refractory digital ulcers and Raynaud’s phenomenon in a 30-year-old woman with systemic sclerosis: Case report and literature review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]