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  1. Article: Corrigendum: Glomerular Endothelial Cell Stress and Cross-Talk With Podocytes in Early Diabetic Kidney Disease.

    Daehn, Ilse Sofia

    Frontiers in medicine

    2018  Volume 5, Page(s) 113

    Abstract: This corrects the article on p. 76 in vol. 5, PMID: 29629372.]. ...

    Abstract [This corrects the article on p. 76 in vol. 5, PMID: 29629372.].
    Language English
    Publishing date 2018-04-26
    Publishing country Switzerland
    Document type Journal Article ; Published Erratum
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2018.00113
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Glomerular Endothelial Cell Stress and Cross-Talk With Podocytes in Early [corrected] Diabetic Kidney Disease.

    Daehn, Ilse Sofia

    Frontiers in medicine

    2018  Volume 5, Page(s) 76

    Abstract: ... of diabetic injury in the kidney, glomerular hypertrophy and podocyte depletion are glomerular hallmarks ... to diabetes and cell cross-talk will provide mechanistic clues that underlie DKD and provide novel avenues ... Diabetic kidney disease (DKD) is one of the major causes of morbidity and mortality in diabetic ...

    Abstract Diabetic kidney disease (DKD) is one of the major causes of morbidity and mortality in diabetic patients and also the leading single cause of end-stage renal disease in the United States. A large proportion of diabetic patients develop DKD and others don't, even with comparable blood glucose levels, indicating a significant genetic component of disease susceptibility. The glomerulus is the primary site of diabetic injury in the kidney, glomerular hypertrophy and podocyte depletion are glomerular hallmarks of progressive DKD, and the degree of podocyte loss correlates with severity of the disease. We know that chronic hyperglycemia contributes to both microvascular and macrovascular complications, as well as podocyte injury. We are beginning to understand the role of glomerular endothelial injury, as well as the involvement of reactive oxygen species and mitochondrial stress, which play a direct role in DKD and in other diabetic complications. There is, however, a gap in our knowledge that links genetic susceptibility to early molecular mechanisms and proteinuria in DKD. Emerging research that explores glomerular cell's specific responses to diabetes and cell cross-talk will provide mechanistic clues that underlie DKD and provide novel avenues for therapeutic intervention.
    Language English
    Publishing date 2018-03-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2018.00076
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Glomerular Endothelial Cell Stress and Cross-Talk With Podocytes in Early Diabetic Kidney Disease

    Ilse Sofia Daehn

    Frontiers in Medicine, Vol

    2018  Volume 5

    Abstract: ... of diabetic injury in the kidney, glomerular hypertrophy and podocyte depletion are glomerular hallmarks ... to diabetes and cell cross-talk will provide mechanistic clues that underlie DKD and provide novel avenues ... Diabetic kidney disease (DKD) is one of the major causes of morbidity and mortality in diabetic ...

    Abstract Diabetic kidney disease (DKD) is one of the major causes of morbidity and mortality in diabetic patients and also the leading single cause of end-stage renal disease in the United States. A large proportion of diabetic patients develop DKD and others don’t, even with comparable blood glucose levels, indicating a significant genetic component of disease susceptibility. The glomerulus is the primary site of diabetic injury in the kidney, glomerular hypertrophy and podocyte depletion are glomerular hallmarks of progressive DKD, and the degree of podocyte loss correlates with severity of the disease. We know that chronic hyperglycemia contributes to both microvascular and macrovascular complications, as well as podocyte injury. We are beginning to understand the role of glomerular endothelial injury, as well as the involvement of reactive oxygen species and mitochondrial stress, which play a direct role in DKD and in other diabetic complications. There is, however, a gap in our knowledge that links genetic susceptibility to early molecular mechanisms and proteinuria in DKD. Emerging research that explores glomerular cell’s specific responses to diabetes and cell cross-talk will provide mechanistic clues that underlie DKD and provide novel avenues for therapeutic intervention.
    Keywords diabetic kidney disease ; glomerulus ; cross-talk ; podocyte ; endothelial cell ; reactive oxygen species ; Medicine (General) ; R5-920
    Subject code 610
    Language English
    Publishing date 2018-03-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Glomerular Endothelial Mitochondrial Dysfunction Is Essential and Characteristic of Diabetic Kidney Disease Susceptibility.

    Qi, Haiying / Casalena, Gabriella / Shi, Shaolin / Yu, Liping / Ebefors, Kerstin / Sun, Yezhou / Zhang, Weijia / D'Agati, Vivette / Schlondorff, Detlef / Haraldsson, Börje / Böttinger, Erwin / Daehn, Ilse

    Diabetes

    2016  Volume 66, Issue 3, Page(s) 763–778

    Abstract: ... progression, and suggest that cross talk between glomerular endothelial injury and podocytes leads to defects ... capillaries from diabetic D2 mice demonstrated early signs of endothelial injury and loss of fenestrae ... of diabetic kidney disease (DKD) remain poorly understood. We compared the early transcriptome profile between DKD-resistant ...

    Abstract The molecular signaling mechanisms between glomerular cell types during initiation/progression of diabetic kidney disease (DKD) remain poorly understood. We compared the early transcriptome profile between DKD-resistant C57BL/6J and DKD-susceptible DBA/2J (D2) glomeruli and demonstrated a significant downregulation of essential mitochondrial genes in glomeruli from diabetic D2 mice, but not in C57BL/6J, with comparable hyperglycemia. Diabetic D2 mice manifested increased mitochondrial DNA lesions (8-oxoguanine) exclusively localized to glomerular endothelial cells after 3 weeks of diabetes, and these accumulated over time in addition to increased urine secretion of 8-oxo-deoxyguanosine. Detailed assessment of glomerular capillaries from diabetic D2 mice demonstrated early signs of endothelial injury and loss of fenestrae. Glomerular endothelial mitochondrial dysfunction was associated with increased glomerular endothelin-1 receptor type A (Ednra) expression and increased circulating endothelin-1 (Edn1). Selective Ednra blockade or mitochondrial-targeted reactive oxygen species scavenging prevented mitochondrial oxidative stress of endothelial cells and ameliorated diabetes-induced endothelial injury, podocyte loss, albuminuria, and glomerulosclerosis. In human DKD, increased urine 8-oxo-deoxyguanosine was associated with rapid DKD progression, and biopsies from patients with DKD showed increased mitochondrial DNA damage associated with glomerular endothelial EDNRA expression. Our studies show that DKD susceptibility was linked to mitochondrial dysfunction, mediated largely by Edn1-Ednra in glomerular endothelial cells representing an early event in DKD progression, and suggest that cross talk between glomerular endothelial injury and podocytes leads to defects and depletion, albuminuria, and glomerulosclerosis.
    MeSH term(s) Adult ; Aged ; Albuminuria ; Animals ; Antioxidants/pharmacology ; Chromatography, High Pressure Liquid ; DNA, Mitochondrial/metabolism ; Deoxyguanosine/analogs & derivatives ; Deoxyguanosine/urine ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 1/metabolism ; Diabetic Nephropathies/metabolism ; Disease Susceptibility ; Endothelin-1/metabolism ; Endothelium/drug effects ; Endothelium/metabolism ; Endothelium/ultrastructure ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Humans ; Kidney Glomerulus/drug effects ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Glomerulus/ultrastructure ; Male ; Mesangial Cells/pathology ; Mesangial Cells/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Microscopy, Electron, Scanning ; Middle Aged ; Mitochondria/drug effects ; Mitochondria/metabolism ; Organophosphorus Compounds/pharmacology ; Oxygen Consumption ; Piperidines/pharmacology ; Podocytes/pathology ; Podocytes/ultrastructure ; Real-Time Polymerase Chain Reaction ; Receptor, Endothelin A/metabolism ; Signal Transduction ; Young Adult
    Chemical Substances Antioxidants ; DNA, Mitochondrial ; Endothelin-1 ; MitoTEMPO ; Organophosphorus Compounds ; Piperidines ; Receptor, Endothelin A ; 8-oxo-7-hydrodeoxyguanosine (88847-89-6) ; Deoxyguanosine (G9481N71RO)
    Language English
    Publishing date 2016-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db16-0695
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Corrigendum

    Ilse Sofia Daehn

    Frontiers in Medicine, Vol

    Glomerular Endothelial Cell Stress and Cross-Talk With Podocytes in Early Diabetic Kidney Disease

    2018  Volume 5

    Keywords diabetic kidney disease ; glomerulus ; crosstalk ; podocyte ; endothelial cell ; ROS ; Medicine (General) ; R5-920
    Language English
    Publishing date 2018-04-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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