Zeisberg, Michael

[["dc.bibliographiccitation.firstpage","2001"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","2008"],["dc.bibliographiccitation.volume","160"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Maeshima, Yohei"],["dc.contributor.author","Mosterman, Barbara"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:12:53Z"],["dc.date.available","2020-11-24T12:12:53Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1016/S0002-9440(10)61150-9"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69166"],["dc.relation.issn","0002-9440"],["dc.title","Renal Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["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.firstpage","264"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Pathology"],["dc.bibliographiccitation.lastpage","273"],["dc.bibliographiccitation.volume","229"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T09:30:53Z"],["dc.date.accessioned","2019-02-19T16:44:38Z"],["dc.date.available","2018-11-07T09:30:53Z"],["dc.date.available","2019-02-19T16:44:38Z"],["dc.date.issued","2013"],["dc.description.abstract","The aberrant methylation of CpG island promoters of selected genes is the prominent epigenetic mechanism by which gene transcription can be effectively silenced. Aberrant hypermethylation of a few selected genes plays an important role in facilitating fibrotic fibroblast activation and in driving fibrogenesis. Here we review mechanisms of DNA methylation and demethylation and their implications for fibroblast activation and tissue fibrosis."],["dc.identifier.doi","10.1002/path.4120"],["dc.identifier.isi","000312542400013"],["dc.identifier.pmid","23097091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31417"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57601"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/78"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","0022-3417"],["dc.relation.issn","1096-9896"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","The role of promoter hypermethylation in fibroblast activation and fibrogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","16002"],["dc.bibliographiccitation.issue","38"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","16007"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","O'Connell, Joyce T."],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Cooke, Vesselina G."],["dc.contributor.author","MacDonald, Brian A."],["dc.contributor.author","Mehta, Ankit I."],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Dewar, Rajan"],["dc.contributor.author","Rocha, Rafael M."],["dc.contributor.author","Brentani, Ricardo R."],["dc.contributor.author","Resnick, Murray B."],["dc.contributor.author","Neilson, Eric G."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:14:08Z"],["dc.date.available","2020-11-24T12:14:08Z"],["dc.date.issued","2011-09-20"],["dc.description.abstract","Increased numbers of S100A4(+) cells are associated with poor prognosis in patients who have cancer. Although the metastatic capabilities of S100A4(+) cancer cells have been examined, the functional role of S100A4(+) stromal cells in metastasis is largely unknown. To study the contribution of S100A4(+) stromal cells in metastasis, we used transgenic mice that express viral thymidine kinase under control of the S100A4 promoter to specifically ablate S100A4(+) stromal cells. Depletion of S100A4(+) stromal cells significantly reduced metastatic colonization without affecting primary tumor growth. Multiple bone marrow transplantation studies demonstrated that these effects of S100A4(+) stromal cells are attributable to local non-bone marrow-derived S100A4(+) cells, which are likely fibroblasts in this setting. Reduction in metastasis due to the loss of S100A4(+) fibroblasts correlated with a concomitant decrease in the expression of several ECM molecules and growth factors, particularly Tenascin-C and VEGF-A. The functional importance of stromal Tenascin-C and S100A4(+) fibroblast-derived VEGF-A in metastasis was established by examining Tenascin-C null mice and transgenic mice expressing Cre recombinase under control of the S100A4 promoter crossed with mice carrying VEGF-A alleles flanked by loxP sites, which exhibited a significant decrease in metastatic colonization without effects on primary tumor growth. In particular, S100A4(+) fibroblast-derived VEGF-A plays an important role in the establishment of an angiogenic microenvironment at the metastatic site to facilitate colonization, whereas stromal Tenascin-C may provide protection from apoptosis. Our study demonstrates a crucial role for local S100A4(+) fibroblasts in providing the permissive \"soil\" for metastatic colonization, a challenging step in the metastatic cascade."],["dc.identifier.doi","10.1073/pnas.1109493108"],["dc.identifier.pmid","21911392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69180"],["dc.language.iso","en"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","VEGF-A and Tenascin-C produced by S100A4+ stromal cells are important for metastatic colonization"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2992"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","2998"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Strutz, Frank M."],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2018-11-07T09:02:29Z"],["dc.date.available","2018-11-07T09:02:29Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1681/ASN.2006050420"],["dc.identifier.isi","000241912100010"],["dc.identifier.pmid","17035610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24690"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","American Society Nephrology"],["dc.relation.issn","1046-6673"],["dc.title","Renal fibroblasts and myofibroblasts in chronic kidney disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5858"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Serin, Nazli; \t\t \r\n\t\t Clinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, nazli.serin@med.uni-goettingen.de\t\t \r\n\t\t Department of Hematology and Oncology, University of Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, nazli.serin@med.uni-goettingen.de"],["dc.contributor.affiliation","Dihazi, Gry H.; \t\t \r\n\t\t Institute of Clinical Chemistry/UMG-Laboratories, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, gryhelene.dihazi@med.uni-goettingen.de"],["dc.contributor.affiliation","Tayyeb, Asima; \t\t \r\n\t\t School of Biological Sciences, University of the Punjab, Lahore 54590, Pakistan, asima.sbs@pu.edu.pk"],["dc.contributor.affiliation","Lenz, Christof; \t\t \r\n\t\t Institute of Clinical Chemistry/UMG-Laboratories, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, christof.lenz@med.uni-goettingen.de\t\t \r\n\t\t Bioanalytical Mass Spectrometry, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany, christof.lenz@med.uni-goettingen.de"],["dc.contributor.affiliation","Müller, Gerhard A.; \t\t \r\n\t\t Clinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, gmueller@med.uni-goettingen.de"],["dc.contributor.affiliation","Zeisberg, Michael; \t\t \r\n\t\t Clinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, michael.zeisberg@med.uni-goettingen.de"],["dc.contributor.affiliation","Dihazi, Hassan; \t\t \r\n\t\t Clinic for Nephrology and Rheumatology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, dihazi@med.uni-goettingen.de\t\t \r\n\t\t Center for Biostructural Imaging of Neurodegeneration (BIN), University Medical Center Göttingen, 37075 Göttingen, Germany, dihazi@med.uni-goettingen.de"],["dc.contributor.author","Serin, Nazli"],["dc.contributor.author","Dihazi, Gry H."],["dc.contributor.author","Tayyeb, Asima"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Dihazi, Hassan"],["dc.date.accessioned","2021-07-05T15:00:46Z"],["dc.date.available","2021-07-05T15:00:46Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-06T07:10:18Z"],["dc.description.abstract","Nephrogenesis is driven by complex signaling pathways that control cell growth and differentiation. The endoplasmic reticulum chaperone calreticulin (Calr) is well known for its function in calcium storage and in the folding of glycoproteins. Its role in kidney development is still not understood. We provide evidence for a pivotal role of Calr in nephrogenesis in this investigation. We show that Calr deficiency results in the disrupted formation of an intact nephrogenic zone and in retardation of nephrogenesis, as evidenced by the disturbance in the formation of comma-shaped and s-shaped bodies. Using proteomics and transcriptomics approaches, we demonstrated that in addition to an alteration in Wnt-signaling key proteins, embryonic kidneys from Calr−/− showed an overall impairment in expression of ribosomal proteins which reveals disturbances in protein synthesis and nephrogenesis. CRISPR/cas9 mediated knockout confirmed that Calr deficiency is associated with a deficiency of several ribosomal proteins and key proteins in ribosome biogenesis. Our data highlights a direct link between Calr expression and the ribosome biogenesis."],["dc.description.abstract","Nephrogenesis is driven by complex signaling pathways that control cell growth and differentiation. The endoplasmic reticulum chaperone calreticulin (Calr) is well known for its function in calcium storage and in the folding of glycoproteins. Its role in kidney development is still not understood. We provide evidence for a pivotal role of Calr in nephrogenesis in this investigation. We show that Calr deficiency results in the disrupted formation of an intact nephrogenic zone and in retardation of nephrogenesis, as evidenced by the disturbance in the formation of comma-shaped and s-shaped bodies. Using proteomics and transcriptomics approaches, we demonstrated that in addition to an alteration in Wnt-signaling key proteins, embryonic kidneys from Calr−/− showed an overall impairment in expression of ribosomal proteins which reveals disturbances in protein synthesis and nephrogenesis. CRISPR/cas9 mediated knockout confirmed that Calr deficiency is associated with a deficiency of several ribosomal proteins and key proteins in ribosome biogenesis. Our data highlights a direct link between Calr expression and the ribosome biogenesis."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/ijms22115858"],["dc.identifier.pii","ijms22115858"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87900"],["dc.language.iso","en"],["dc.notes.intern","DOI Import DOI-Import GROB-441"],["dc.relation.eissn","1422-0067"],["dc.relation.orgunit","Klinik für Nephrologie und Rheumatologie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Calreticulin Deficiency Disturbs Ribosome Biogenesis and Results in Retardation in Embryonic Kidney Development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","256"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","264"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Yang, Changqing"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Soubasakos, Mary A."],["dc.contributor.author","Giraldo, Mauricio"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:14:44Z"],["dc.date.available","2020-11-24T12:14:44Z"],["dc.date.issued","2007-01"],["dc.description.abstract","Bone morphogenic protein-7 (BMP-7) is a key protein involved in liver organogenesis and development. The physiological circulating concentration of BMP-7 is between 100 and 300 pg/ml. BMP-7 expression is absent in the liver, but the receptors for BMP-7 are present on adult hepatocytes. Therefore, we hypothesized that BMP-7 might function as an endogenous regulator of adult hepatocyte proliferation and liver homeostasis. Here, we demonstrate that neutralization of circulating endogenous BMP-7 results in significantly impaired regeneration of the liver after partial hepatectomy. Therapeutic administration of recombinant human BMP-7 (rhBMP-7) significantly enhances liver regeneration associated with accelerated improvement of liver function. Collectively, our results argue for the role of BMP-7 as a kidney- and bone-produced endogenous regulator of hepatocyte health."],["dc.identifier.doi","10.1096/fj.06-6837com"],["dc.identifier.pmid","17116741"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69188"],["dc.language.iso","en"],["dc.relation.eissn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.title","BMP-7 functions as a novel hormone to facilitate liver regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","16"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2019-07-09T11:41:46Z"],["dc.date.available","2019-07-09T11:41:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Based on extensive pre-clinical achievements over the past decades, it appears to be due time for a successful clinical translation in the renal fibrosis field—but what is the quickest road to get there? In light of the recent launch of the Precision Medicine Initiative and success of molecularly informed drugs in oncology, we here discuss what it may take to bring molecularly targeted anti-fibrotic to clinical use in chronic progressive kidney disease."],["dc.identifier.doi","10.1186/s13069-015-0033-x"],["dc.identifier.pmid","26330891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58506"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Precision renal medicine: a roadmap towards targeted kidney fibrosis therapies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","31154"],["dc.bibliographiccitation.issue","34"],["dc.bibliographiccitation.journal","The Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","31162"],["dc.bibliographiccitation.volume","277"],["dc.contributor.author","Hamano, Yuki"],["dc.contributor.author","Grunkemeyer, James A."],["dc.contributor.author","Sudhakar, Akulapalli"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Cosgrove, Dominic"],["dc.contributor.author","Morello, Roy"],["dc.contributor.author","Lee, Brendan"],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2020-11-24T12:14:18Z"],["dc.date.available","2020-11-24T12:14:18Z"],["dc.date.issued","2002-08-23"],["dc.description.abstract","The human kidneys filter 70 liters of blood plasma every day. The hallmark of almost all kidney diseases, whether acquired or genetic, is the leakage of plasma proteins into the urine because of alterations in the glomerular filtration unit of the kidney. In this regard, the human mutations in nephrin, podocin, alpha-actinin-4, COL4A3, and COL4A5 genes expressed in the glomeruli have been implicated to cause alterations in glomerular filtration apparatus. Nevertheless, the expression of these proteins in relation to each other in mouse models for glomerular vascular leak is unknown. Additionally, within the glomerulus, the central question of whether the primary filtration barrier is the basement membrane or the epithelial slit diaphragm remains ambiguous. Therefore, in this study, we examined the localization and expression of glomerular epithelial slit diaphragm and glomerular basement membrane proteins implicated in glomerular vascular leak using mice deficient in either the alpha3 chain of type IV collagen, the major constituent of glomerular basement membrane, or LMX1B transcription factor, which regulates the expression of key glomerular type IV collagen genes COL4A3 and COL4A4 or nephrin, a glomerular epithelial slit diaphragm-associated protein. This study demonstrates that decreased expression of slit diaphragm protein, nephrin, correlates with a loss of glomerular filter integrity. Additionally, we demonstrate that defects induced by proteins of glomerular basement membrane lead to an insidious plasma protein leak, whereas the defects induced by proteins in the glomerular epithelial slit diaphragms lead to a precipitous plasma protein leak."],["dc.identifier.doi","10.1074/jbc.M204806200"],["dc.identifier.pmid","12039968"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69182"],["dc.language.iso","en"],["dc.relation.issn","0021-9258"],["dc.title","Determinants of vascular permeability in the kidney glomerulus"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","629"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Seminars in nephrology"],["dc.bibliographiccitation.lastpage","636"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Hulshoff, Melanie S."],["dc.contributor.author","Rath, Sandip K."],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.date.accessioned","2020-11-24T12:13:03Z"],["dc.date.available","2020-11-24T12:13:03Z"],["dc.date.issued","2018"],["dc.description.abstract","Cardiovascular disease and heart failure are the primary cause of morbidity and mortality in patients with chronic kidney disease. Because impairment of kidney function correlates with heart failure and cardiac fibrosis, a kidney-heart axis is suspected. Although our understanding of the underlying mechanisms still is evolving, the possibility that kidney-heart messengers could be intercepted offers ample reason to focus on this clinically highly relevant problem. Here, we review the current knowledge of how kidney injury causes heart failure and fibrosis."],["dc.identifier.doi","10.1016/j.semnephrol.2018.08.007"],["dc.identifier.pmid","30413256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69168"],["dc.language.iso","en"],["dc.relation.eissn","1558-4488"],["dc.relation.issn","0270-9295"],["dc.title","Causal Connections From Chronic Kidney Disease to Cardiac Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]