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  1. AU="Daehn, Ilse S"
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  1. Article ; Online: Mitochondria Matter: A Critical Role of

    Daehn, Ilse S

    Journal of the American Society of Nephrology : JASN

    2020  Volume 31, Issue 6, Page(s) 1167–1169

    MeSH term(s) Humans ; Hydroxybenzoates ; Mitochondria ; Nephrotic Syndrome/drug therapy ; Podocytes ; Steroids ; Ubiquinone
    Chemical Substances Hydroxybenzoates ; Steroids ; Ubiquinone (1339-63-5) ; beta-resorcylic acid (LU39SC9JYL)
    Language English
    Publishing date 2020-05-07
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2020040467
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3344: Show issues Location:
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  2. Article ; Online: Insights into glomerular function and disease pathogenesis.

    Lassén, Emelie / Daehn, Ilse S

    Nature reviews. Nephrology

    2022  Volume 19, Issue 2, Page(s) 85–86

    MeSH term(s) Humans ; Kidney Glomerulus/pathology ; Nephrotic Syndrome/pathology
    Language English
    Publishing date 2022-12-17
    Publishing country England
    Document type Journal Article
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-022-00667-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Hypertrophy and glomerular cell adaptation through crosstalk leads to glomerular injury after kidney transplantation.

    Lassen, Emelie / Daehn, Ilse S

    Kidney international

    2022  Volume 101, Issue 4, Page(s) 673–676

    Abstract: Menon et al. report cell-specific transcriptional changes in podocytes and glomerular endothelial cells that indicate cell stress and increased bidirectional crosstalk among these cells in apparently healthy human allografts. They identified common and ... ...

    Abstract Menon et al. report cell-specific transcriptional changes in podocytes and glomerular endothelial cells that indicate cell stress and increased bidirectional crosstalk among these cells in apparently healthy human allografts. They identified common and independent podocytes and glomerular endothelial cell-specific responses in nondiabetic and diabetic transplant recipients, as well as parallels in genes related to podocyte and glomerular endothelial cell stress in experimental focal segmental glomerular sclerosis. These findings could explain hypertrophy-associated glomerular disease progression associated with podocyte detachment after transplantation.
    MeSH term(s) Endothelial Cells ; Female ; Glomerulosclerosis, Focal Segmental/genetics ; Humans ; Hypertrophy ; Kidney Diseases ; Kidney Glomerulus ; Kidney Transplantation/adverse effects ; Male ; Podocytes
    Language English
    Publishing date 2022-04-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2022.01.008
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  4. Article: Editorial: Molecular mechanisms of proteinuria, volume II.

    Daehn, Ilse S / Merscher, Sandra

    Frontiers in medicine

    2022  Volume 9, Page(s) 1026202

    Language English
    Publishing date 2022-10-13
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2022.1026202
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  5. Article ; Online: Tackling chronic kidney disease in diabetic patients with finerenone.

    Das, Bhaskar / Daehn, Ilse S

    Trends in pharmacological sciences

    2022  Volume 43, Issue 9, Page(s) 799–800

    MeSH term(s) Diabetes Mellitus, Type 2 ; Humans ; Naphthyridines ; Renal Insufficiency, Chronic/drug therapy
    Chemical Substances Naphthyridines ; finerenone
    Language English
    Publishing date 2022-06-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2022.05.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Redox regulation in diabetic kidney disease.

    Daehn, Ilse S / Ekperikpe, Ubong S / Stadler, Krisztian

    American journal of physiology. Renal physiology

    2023  Volume 325, Issue 2, Page(s) F135–F149

    Abstract: Diabetic kidney disease (DKD) is one of the most devastating complications of diabetes mellitus, where currently there is no cure available. Several important mechanisms contribute to the pathogenesis of this complication, with oxidative stress being one ...

    Abstract Diabetic kidney disease (DKD) is one of the most devastating complications of diabetes mellitus, where currently there is no cure available. Several important mechanisms contribute to the pathogenesis of this complication, with oxidative stress being one of the key factors. The past decades have seen a large number of publications with various aspects of this topic; however, the specific details of redox regulation in DKD are still unclear. This is partly because redox biology is very complex, coupled with a complex and heterogeneous organ with numerous cell types. Furthermore, often times terms such as "oxidative stress" or reactive oxygen species are used as a general term to cover a wide and rich variety of reactive species and their differing reactions. However, no reactive species are the same, and not all of them are capable of biologically relevant reactions or "redox signaling." The goal of this review is to provide a biochemical background for an array of specific reactive oxygen species types with varying reactivity and specificity in the kidney as well as highlight some of the advances in redox biology that are paving the way to a better understanding of DKD development and risk.
    MeSH term(s) Humans ; Diabetic Nephropathies/metabolism ; Reactive Oxygen Species/metabolism ; Oxidative Stress/physiology ; Kidney/metabolism ; Oxidation-Reduction ; Diabetes Mellitus/metabolism
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2023-06-01
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00047.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Clues to Glomerular Cell Chatter in

    Lassén, Emelie / Daehn, Ilse S

    Kidney international reports

    2021  Volume 6, Issue 7, Page(s) 1758–1760

    Language English
    Publishing date 2021-05-20
    Publishing country United States
    Document type Editorial
    ISSN 2468-0249
    ISSN (online) 2468-0249
    DOI 10.1016/j.ekir.2021.05.013
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  8. Article ; Online: Disability innovation strengthens STEM.

    Daehn, Ilse S / Croxson, Paula L

    Science (New York, N.Y.)

    2021  Volume 373, Issue 6559, Page(s) 1097–1099

    Language English
    Publishing date 2021-09-01
    Publishing country United States
    Document type Letter
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abk2631
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    Zs.MG 77: Show issues

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  9. Article ; Online: The glomerular filtration barrier: a structural target for novel kidney therapies.

    Daehn, Ilse S / Duffield, Jeremy S

    Nature reviews. Drug discovery

    2021  Volume 20, Issue 10, Page(s) 770–788

    Abstract: Loss of normal kidney function affects more than 10% of the population and contributes to morbidity and mortality. Kidney diseases are currently treated with immunosuppressive agents, antihypertensives and diuretics with partial but limited success. Most ...

    Abstract Loss of normal kidney function affects more than 10% of the population and contributes to morbidity and mortality. Kidney diseases are currently treated with immunosuppressive agents, antihypertensives and diuretics with partial but limited success. Most kidney disease is characterized by breakdown of the glomerular filtration barrier (GFB). Specialized podocyte cells maintain the GFB, and structure-function experiments and studies of intercellular communication between the podocytes and other GFB cells, combined with advances from genetics and genomics, have laid the groundwork for a new generation of therapies that directly intervene at the GFB. These include inhibitors of apolipoprotein L1 (APOL1), short transient receptor potential channels (TRPCs), soluble fms-like tyrosine kinase 1 (sFLT1; also known as soluble vascular endothelial growth factor receptor 1), roundabout homologue 2 (ROBO2), endothelin receptor A, soluble urokinase plasminogen activator surface receptor (suPAR) and substrate intermediates for coenzyme Q10 (CoQ
    MeSH term(s) Animals ; Glomerular Filtration Barrier/drug effects ; Glomerular Filtration Barrier/physiology ; Glomerular Filtration Barrier/physiopathology ; Humans ; Kidney Diseases/drug therapy ; Kidney Diseases/physiopathology
    Language English
    Publishing date 2021-07-14
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062954-0
    ISSN 1474-1784 ; 1474-1776
    ISSN (online) 1474-1784
    ISSN 1474-1776
    DOI 10.1038/s41573-021-00242-0
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    Zs.MO 334: Show issues
    Zs.MG 63: Show issues

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  10. Article ; Online: Podocyte as the link between sterile inflammation and diabetic kidney disease.

    Lassén, Emelie / Bouchareb, Rihab / Daehn, Ilse S

    Kidney international

    2022  Volume 102, Issue 4, Page(s) 688–690

    Abstract: Shahzad et al. examined the underlying mechanisms of sterile inflammation in diabetic kidney disease, specifically the role of NLRP3 inflammasome activation in podocytes. Using mouse models with gain-of-function and loss-of-function mutations in podocyte ...

    Abstract Shahzad et al. examined the underlying mechanisms of sterile inflammation in diabetic kidney disease, specifically the role of NLRP3 inflammasome activation in podocytes. Using mouse models with gain-of-function and loss-of-function mutations in podocyte Nlrp3, or caspase-1 loss-of-function mutations in podocytes, they identified that Nlrp3 activation in these cells is central for development of diabetic kidney disease but not solely dependent on canonical mechanisms and caspase-1. These findings position podocyte-mediated immune cell-like functions as potential therapeutic targets for diabetic kidney disease.
    MeSH term(s) Animals ; Caspases ; Diabetes Mellitus ; Diabetic Nephropathies/genetics ; Inflammasomes ; Inflammation ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Podocytes
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2022-09-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2022.07.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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