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  1. Article ; Online: "Idiopathic" minimal change nephrotic syndrome: a podocyte mystery nears the end.

    Chugh, Sumant S / Clement, Lionel C

    American journal of physiology. Renal physiology

    2023  Volume 325, Issue 6, Page(s) F685–F694

    Abstract: The discovery of zinc fingers and homeoboxes (ZHX) transcriptional factors and the upregulation of hyposialylated angiopoietin-like 4 (ANGPTL4) in podocytes have been crucial in explaining the cardinal manifestations of human minimal change nephrotic ... ...

    Abstract The discovery of zinc fingers and homeoboxes (ZHX) transcriptional factors and the upregulation of hyposialylated angiopoietin-like 4 (ANGPTL4) in podocytes have been crucial in explaining the cardinal manifestations of human minimal change nephrotic syndrome (MCNS). Recently, uncovered genomic defects upstream of
    MeSH term(s) Mice ; Humans ; Animals ; Nephrosis, Lipoid/drug therapy ; Podocytes/metabolism ; Common Cold/metabolism ; Proteinuria/metabolism ; Glomerular Basement Membrane/metabolism ; Recurrence ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/metabolism ; Transcription Factors/metabolism ; Homeodomain Proteins/metabolism
    Chemical Substances ZHX2 protein, human ; Transcription Factors ; Homeodomain Proteins
    Language English
    Publishing date 2023-10-05
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00219.2023
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  2. Article ; Online: Cytokine storm-based mechanisms for extrapulmonary manifestations of SARS-CoV-2 infection.

    Del Nogal Avila, Maria / Das, Ranjan / Kharlyngdoh, Joubert / Molina-Jijon, Eduardo / Donoro Blazquez, Hector / Gambut, Stéphanie / Crowley, Michael / Crossman, David K / Gbadegesin, Rasheed A / Chugh, Sunveer S / Chugh, Sunjeet S / Avila-Casado, Carmen / Macé, Camille / Clement, Lionel C / Chugh, Sumant S

    JCI insight

    2023  Volume 8, Issue 10

    Abstract: Viral illnesses like SARS-CoV-2 have pathologic effects on nonrespiratory organs in the absence of direct viral infection. We injected mice with cocktails of rodent equivalents of human cytokine storms resulting from SARS-CoV-2/COVID-19 or rhinovirus ... ...

    Abstract Viral illnesses like SARS-CoV-2 have pathologic effects on nonrespiratory organs in the absence of direct viral infection. We injected mice with cocktails of rodent equivalents of human cytokine storms resulting from SARS-CoV-2/COVID-19 or rhinovirus common cold infection. At low doses, COVID-19 cocktails induced glomerular injury and albuminuria in zinc fingers and homeoboxes 2 (Zhx2) hypomorph and Zhx2+/+ mice to mimic COVID-19-related proteinuria. Common Cold cocktail induced albuminuria selectively in Zhx2 hypomorph mice to model relapse of minimal change disease, which improved after depletion of TNF-α, soluble IL-4Rα, or IL-6. The Zhx2 hypomorph state increased cell membrane to nuclear migration of podocyte ZHX proteins in vivo (both cocktails) and lowered phosphorylated STAT6 activation (COVID-19 cocktail) in vitro. At higher doses, COVID-19 cocktails induced acute heart injury, myocarditis, pericarditis, acute liver injury, acute kidney injury, and high mortality in Zhx2+/+ mice, whereas Zhx2 hypomorph mice were relatively protected, due in part to early, asynchronous activation of STAT5 and STAT6 pathways in these organs. Dual depletion of cytokine combinations of TNF-α with IL-2, IL-13, or IL-4 in Zhx2+/+ mice reduced multiorgan injury and eliminated mortality. Using genome sequencing and CRISPR/Cas9, an insertion upstream of ZHX2 was identified as a cause of the human ZHX2 hypomorph state.
    MeSH term(s) Humans ; Mice ; Animals ; Homeodomain Proteins/genetics ; Albuminuria ; Tumor Necrosis Factor-alpha ; Common Cold ; Cytokine Release Syndrome ; COVID-19 ; SARS-CoV-2/metabolism ; Transcription Factors/genetics
    Chemical Substances Homeodomain Proteins ; Tumor Necrosis Factor-alpha ; ZHX2 protein, human ; Transcription Factors
    Language English
    Publishing date 2023-05-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.166012
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  3. Article ; Online: Cytokine storm–based mechanisms for extrapulmonary manifestations of SARS-CoV-2 infection

    Maria Del Nogal Avila / Ranjan Das / Joubert Kharlyngdoh / Eduardo Molina-Jijon / Hector Donoro Blazquez / Stéphanie Gambut / Michael Crowley / David K. Crossman / Rasheed A. Gbadegesin / Sunveer S. Chugh / Sunjeet S. Chugh / Carmen Avila-Casado / Camille Macé / Lionel C. Clement / Sumant S. Chugh

    JCI Insight, Vol 8, Iss

    2023  Volume 10

    Abstract: Viral illnesses like SARS-CoV-2 have pathologic effects on nonrespiratory organs in the absence of direct viral infection. We injected mice with cocktails of rodent equivalents of human cytokine storms resulting from SARS-CoV-2/COVID-19 or rhinovirus ... ...

    Abstract Viral illnesses like SARS-CoV-2 have pathologic effects on nonrespiratory organs in the absence of direct viral infection. We injected mice with cocktails of rodent equivalents of human cytokine storms resulting from SARS-CoV-2/COVID-19 or rhinovirus common cold infection. At low doses, COVID-19 cocktails induced glomerular injury and albuminuria in zinc fingers and homeoboxes 2 (Zhx2) hypomorph and Zhx2+/+ mice to mimic COVID-19–related proteinuria. Common Cold cocktail induced albuminuria selectively in Zhx2 hypomorph mice to model relapse of minimal change disease, which improved after depletion of TNF-α, soluble IL-4Rα, or IL-6. The Zhx2 hypomorph state increased cell membrane to nuclear migration of podocyte ZHX proteins in vivo (both cocktails) and lowered phosphorylated STAT6 activation (COVID-19 cocktail) in vitro. At higher doses, COVID-19 cocktails induced acute heart injury, myocarditis, pericarditis, acute liver injury, acute kidney injury, and high mortality in Zhx2+/+ mice, whereas Zhx2 hypomorph mice were relatively protected, due in part to early, asynchronous activation of STAT5 and STAT6 pathways in these organs. Dual depletion of cytokine combinations of TNF-α with IL-2, IL-13, or IL-4 in Zhx2+/+ mice reduced multiorgan injury and eliminated mortality. Using genome sequencing and CRISPR/Cas9, an insertion upstream of ZHX2 was identified as a cause of the human ZHX2 hypomorph state.
    Keywords Nephrology ; Medicine ; R
    Language English
    Publishing date 2023-05-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Withdrawal: Isolation and functional analysis of mouse UbA52 gene and its relevance to diabetic nephropathy.

    Sun, Lin / Pan, Xiaomin / Wada, Jun / Haas, Christian S / Wuthrich, Rudolf P / Danesh, Farhad R / Chugh, Sumant S / Kanwar, Yashpal S

    The Journal of biological chemistry

    2019  Volume 294, Issue 26, Page(s) 10382

    Language English
    Publishing date 2019-06-28
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.W119.009588
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  5. Article ; Online: Nephrotic syndrome: components, connections, and angiopoietin-like 4-related therapeutics.

    Macé, Camille / Chugh, Sumant S

    Journal of the American Society of Nephrology : JASN

    2014  Volume 25, Issue 11, Page(s) 2393–2398

    Abstract: Nephrotic syndrome is recognized by the presence of proteinuria in excess of 3.5 g/24 h along with hypoalbuminemia, edema, hyperlipidemia (hypertriglyceridemia and hypercholesterolemia), and lipiduria. Each component has been investigated individually ... ...

    Abstract Nephrotic syndrome is recognized by the presence of proteinuria in excess of 3.5 g/24 h along with hypoalbuminemia, edema, hyperlipidemia (hypertriglyceridemia and hypercholesterolemia), and lipiduria. Each component has been investigated individually over the past four decades with some success. Studies published recently have started unraveling the molecular basis of proteinuria and its relationship with other components. We now have improved understanding of the threshold for nephrotic-range proteinuria and the pathogenesis of hypertriglyceridemia. These studies reveal that modifying sialylation of the soluble glycoprotein angiopoietin-like 4 or changing key amino acids in its sequence can be used successfully to treat proteinuria. Treatment strategies on the basis of fundamental relationships among different components of nephrotic syndrome use naturally occurring pathways and have great potential for future development into clinically relevant therapeutic agents.
    MeSH term(s) Angiopoietin-like 4 Protein ; Angiopoietins/genetics ; Angiopoietins/metabolism ; Drug Design ; Humans ; Hyperlipidemias/drug therapy ; Hyperlipidemias/genetics ; Hyperlipidemias/metabolism ; N-Acetylneuraminic Acid/metabolism ; Nephrotic Syndrome/drug therapy ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/metabolism
    Chemical Substances ANGPTL4 protein, human ; Angiopoietin-like 4 Protein ; Angiopoietins ; N-Acetylneuraminic Acid (GZP2782OP0)
    Language English
    Publishing date 2014-05-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2014030267
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  6. Article ; Online: Withdrawal: High glucose stimulates synthesis of fibronectin via a novel protein kinase C, Rap1b, and B-Raf signaling pathway.

    Lin, Sun / Sahai, Atul / Chugh, Sumant S / Pan, Xiaomin / Wallner, Elisabeth I / Danesh, Farhad R / Lomasney, Jon W / Kanwar, Yashpal S

    The Journal of biological chemistry

    2019  Volume 294, Issue 26, Page(s) 10381

    Language English
    Publishing date 2019-06-28
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.W119.009587
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  7. Article ; Online: Telomerase at the center of collapsing glomerulopathy.

    Chugh, Sumant S / Clement, Lionel C

    Nature medicine

    2012  Volume 18, Issue 1, Page(s) 26–27

    MeSH term(s) AIDS-Associated Nephropathy/metabolism ; Animals ; Humans ; Kidney/metabolism ; Kidney Glomerulus/metabolism ; Podocytes/cytology ; Telomerase/metabolism ; Wnt Signaling Pathway
    Chemical Substances Telomerase (EC 2.7.7.49) ; Tert protein, mouse (EC 2.7.7.49)
    Language English
    Publishing date 2012-01-06
    Publishing country United States
    Document type News ; Comment
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm.2602
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  8. Article: Transcriptional regulation of podocyte disease.

    Chugh, Sumant S

    Translational research : the journal of laboratory and clinical medicine

    2007  Volume 149, Issue 5, Page(s) 237–242

    Abstract: The podocyte is a highly specialized visceral epithelial cell that forms the outermost layer of the glomerular capillary loop and plays a critical role in the maintenance of the glomerular filtration barrier. Several transcriptional factors regulate the ... ...

    Abstract The podocyte is a highly specialized visceral epithelial cell that forms the outermost layer of the glomerular capillary loop and plays a critical role in the maintenance of the glomerular filtration barrier. Several transcriptional factors regulate the podocyte function under normal and disease conditions. In this review, the role of Wilms tumor 1 (WT1), LIM homeobox transcription factor 1, beta (Lmx1b), pod1, pax-2, kreisler, nuclear factor-kappa B (NF-kappaB), smad7, and zinc fingers and homeoboxes (ZHX) proteins in the development of podocyte disease is outlined. The regulation of several important podocyte genes, including transcriptional factors, by ZHX proteins, their predominant non-nuclear localization in the normal in vivo podocyte, and changes in ZHX expression related to the development of minimal change disease and focal and segmental glomerulosclerosis are discussed. Finally, some future therapeutic strategies for glomerular disease are proposed.
    MeSH term(s) Animals ; Gene Expression Regulation ; Humans ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Podocytes/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2007-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2246684-8
    ISSN 1878-1810 ; 1532-6543 ; 1931-5244
    ISSN (online) 1878-1810 ; 1532-6543
    ISSN 1931-5244
    DOI 10.1016/j.trsl.2007.01.002
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  9. Article: Coagulase-negative staphylococcus-oftentimes a virulent masquerader.

    Saxena, Nakshatra / Chugh, Sumant S / Centor, Robert

    NDT plus

    2010  Volume 4, Issue 1, Page(s) 81–82

    Language English
    Publishing date 2010-10-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 2410383-4
    ISSN 1753-0784
    ISSN 1753-0784
    DOI 10.1093/ndtplus/sfq185
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  10. Article ; Online: New insights into human minimal change disease: lessons from animal models.

    Chugh, Sumant S / Clement, Lionel C / Macé, Camille

    American journal of kidney diseases : the official journal of the National Kidney Foundation

    2011  Volume 59, Issue 2, Page(s) 284–292

    Abstract: The pathogenesis of minimal change disease (MCD), considered to be the simplest form of nephrotic syndrome, has been one of the major unsolved mysteries in kidney disease. In this review, recent landmark studies that have led to the unraveling of MCD are ...

    Abstract The pathogenesis of minimal change disease (MCD), considered to be the simplest form of nephrotic syndrome, has been one of the major unsolved mysteries in kidney disease. In this review, recent landmark studies that have led to the unraveling of MCD are discussed. A recent study now explains the molecular basis of major clinical and morphologic changes in MCD. Overproduction of angiopoietin-like 4 (ANGPTL4) in podocytes in MCD causes binding of ANGPTL4 to the glomerular basement membrane, development of nephrotic-range selective proteinuria, diffuse effacement of foot processes, and loss of glomerular basement membrane charge, but is not associated with changes shown by light microscopy in the glomerular and tubulointerstitial compartments. At least some of this ability of ANGPTL4 to induce proteinuria is linked to a deficiency of sialic acid residues because oral supplementation with sialic acid precursor N-acetyl-d-mannosamine improves sialylation of podocyte-secreted ANGPTL4 and significantly decreases proteinuria. Animal models of MCD, recent advances in potential biomarkers, and studies of upstream factors that may initiate glomerular changes also are discussed. In summary, recent progress in understanding MCD is likely to influence the diagnosis and treatment of MCD in the near future.
    MeSH term(s) Angiopoietin-like 4 Protein ; Angiopoietins/genetics ; Angiopoietins/metabolism ; Angiopoietins/physiology ; Animals ; Disease Models, Animal ; Glucocorticoids/therapeutic use ; Humans ; Male ; Nephrosis, Lipoid/drug therapy ; Nephrosis, Lipoid/etiology ; Nephrosis, Lipoid/physiopathology ; Prednisone/therapeutic use ; Rats ; Rats, Transgenic ; Treatment Outcome ; Young Adult
    Chemical Substances ANGPTL4 protein, human ; ANGPTL4 protein, rat ; Angiopoietin-like 4 Protein ; Angiopoietins ; Glucocorticoids ; Prednisone (VB0R961HZT)
    Language English
    Publishing date 2011-10-05
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 604539-x
    ISSN 1523-6838 ; 0272-6386
    ISSN (online) 1523-6838
    ISSN 0272-6386
    DOI 10.1053/j.ajkd.2011.07.024
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