Frese, Jenny

[["dc.bibliographiccitation.firstpage","1329"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Tayyeb, Asima; 1School of Biological Sciences, University of the Punjab, Lahore 53700, Pakistan; asima.sbs@pu.edu.pkm"],["dc.contributor.affiliation","Dihazi, Gry H.; 2UMG-Laboratories, Institute for Clinical Chemistry, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; gryhelene.dihazi@med.uni-goettingen.de"],["dc.contributor.affiliation","Tampe, Björn; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Zeisberg, Michael; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Tampe, Desiree; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Hakroush, Samy; 4Department of Pathology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; samy.hakroush@googlemail.com"],["dc.contributor.affiliation","Bührig, Charlotte; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Frese, Jenny; 5Department of Occupational Medicine and Health Safety, Deutsche Post AG, Kölnische Strasse 81, 34117 Kassel, Germany; jenny.frese@med.uni-goettingen.de"],["dc.contributor.affiliation","Serin, Nazli; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Eltoweissy, Marwa; 7Department of Zoology, Faculty of Science, Alexandria University, Alexandria 21568, Egypt; marwaeltoweissy@alexu.edu.eg"],["dc.contributor.affiliation","Müller, Gerhard A.; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.affiliation","Dihazi, Hassan; 3Clinic for Nephrology and Rheumatology, University Medical Centre Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany; bjoern.tampe@med.uni-goettingen.de (B.T.); michael.zeisberg@med.uni-goettingen.de (M.Z.); desiree.tampe@med.uni-goettingen.de (D.T.); charlotte.buehrig@gmx.de (C.B.); nazli.serin@med.uni-goettingen.de (N.S.); gmueller@med.uni-goettingen.de (G.A.M.)"],["dc.contributor.author","Tayyeb, Asima"],["dc.contributor.author","Dihazi, Gry H."],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Bührig, Charlotte"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Serin, Nazli"],["dc.contributor.author","Eltoweissy, Marwa"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Müller, Gerhard A."],["dc.date.accessioned","2022-05-02T08:09:34Z"],["dc.date.available","2022-05-02T08:09:34Z"],["dc.date.issued","2022"],["dc.date.updated","2022-05-05T12:28:41Z"],["dc.description.abstract","Renal Ca2+ reabsorption plays a central role in the fine-tuning of whole-body Ca2+ homeostasis. Here, we identified calreticulin (Calr) as a missing link in Ca2+ handling in the kidney and showed that a shortage of Calr results in mitochondrial disease and kidney pathogenesis. We demonstrated that Calr+/− mice displayed a chronic physiological low level of Calr and that this was associated with progressive renal injury manifested in glomerulosclerosis and tubulointerstitial damage. We found that Calr+/− kidney cells suffer from a disturbance in functionally active calcium stores and decrease in Ca2+ storage capacity. Consequently, the kidney cells displayed an abnormal activation of Ca2+ signaling and NF-κB pathways, resulting in inflammation and wide progressive kidney injury. Interestingly, the disturbance in the Ca2+ homeostasis and signaling in Calr+/− kidney mice cells triggered severe mitochondrial disease and aberrant mitophagy, resulting in a high level of oxidative stress and energy shortage. These findings provide novel mechanistic insight into the role of Calr in kidney calcium handling, function, and pathogenesis."],["dc.description.abstract","Renal Ca2+ reabsorption plays a central role in the fine-tuning of whole-body Ca2+ homeostasis. Here, we identified calreticulin (Calr) as a missing link in Ca2+ handling in the kidney and showed that a shortage of Calr results in mitochondrial disease and kidney pathogenesis. We demonstrated that Calr+/− mice displayed a chronic physiological low level of Calr and that this was associated with progressive renal injury manifested in glomerulosclerosis and tubulointerstitial damage. We found that Calr+/− kidney cells suffer from a disturbance in functionally active calcium stores and decrease in Ca2+ storage capacity. Consequently, the kidney cells displayed an abnormal activation of Ca2+ signaling and NF-κB pathways, resulting in inflammation and wide progressive kidney injury. Interestingly, the disturbance in the Ca2+ homeostasis and signaling in Calr+/− kidney mice cells triggered severe mitochondrial disease and aberrant mitophagy, resulting in a high level of oxidative stress and energy shortage. These findings provide novel mechanistic insight into the role of Calr in kidney calcium handling, function, and pathogenesis."],["dc.identifier.doi","10.3390/cells11081329"],["dc.identifier.pii","cells11081329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107412"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","2073-4409"],["dc.title","Calreticulin Shortage Results in Disturbance of Calcium Storage, Mitochondrial Disease, and Kidney Injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]