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  1. Article ; Online: Phenotypes of APOL1 High-Risk Status Subjects.

    Kopp, Jeffrey B / Yoshida, Teruhiko

    Journal of the American Society of Nephrology : JASN

    2023  Volume 34, Issue 5, Page(s) 735–736

    MeSH term(s) Apolipoprotein L1/genetics ; Phenotype ; Genotype ; Apolipoproteins/genetics
    Chemical Substances Apolipoprotein L1 ; Apolipoproteins
    Language English
    Publishing date 2023-04-29
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.0000000000000123
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    Zs.A 3344: Show issues Location:
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  2. Article ; Online: Disaster preparedness for patients with kidney disease.

    Kopp, Jeffrey B / Lempert, Kenneth / Finne, Kristen

    Nature reviews. Nephrology

    2023  Volume 19, Issue 3, Page(s) 147–148

    MeSH term(s) Humans ; Disasters ; Kidney Diseases ; Patients
    Language English
    Publishing date 2023-02-01
    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/s41581-023-00678-0
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    Zs.MG 107: Show issues

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  3. Article ; Online: APOL1, Acidity, and ATP: Affecting Mitochondrial Function.

    Kopp, Jeffrey B

    American journal of nephrology

    2020  Volume 51, Issue 9, Page(s) 693–694

    MeSH term(s) Adenosine Triphosphate ; Apolipoprotein L1 ; Heartburn ; Humans ; Mitochondria
    Chemical Substances APOL1 protein, human ; Apolipoprotein L1 ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2020-09-03
    Publishing country Switzerland
    Document type Editorial ; Research Support, N.I.H., Intramural ; Comment
    ZDB-ID 604540-6
    ISSN 1421-9670 ; 0250-8095
    ISSN (online) 1421-9670
    ISSN 0250-8095
    DOI 10.1159/000509990
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    Zs.A 1635: Show issues Location:
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  4. Article ; Online: The complexity of nicotinamide adenine dinucleotide (NAD), hypoxic, and aryl hydrocarbon receptor cell signaling in chronic kidney disease.

    Curran, Colleen S / Kopp, Jeffrey B

    Journal of translational medicine

    2023  Volume 21, Issue 1, Page(s) 706

    Abstract: Early-stage detection of chronic kidney diseases (CKD) is important to treatment that may slow and occasionally halt CKD progression. CKD of diverse etiologies share similar histologic patterns of glomerulosclerosis, tubular atrophy, and interstitial ... ...

    Abstract Early-stage detection of chronic kidney diseases (CKD) is important to treatment that may slow and occasionally halt CKD progression. CKD of diverse etiologies share similar histologic patterns of glomerulosclerosis, tubular atrophy, and interstitial fibrosis. Macro-vascular disease and micro-vascular disease promote tissue ischemia, contributing to injury. Tissue ischemia promotes hypoxia, and this in turn activates the hypoxia-inducible transcription factors (HIFs). HIF-1α and HIF-2α, share a dimer partner, HIF-1β, with the aryl hydrocarbon receptor (AHR) and are each activated in CKD and associated with kidney cellular nicotinamide adenine dinucleotide (NAD) depletion. The Preiss-Handler, salvage, and de novo pathways regulate NAD biosynthesis and gap-junctions regulate NAD cellular retention. In the Preiss-Handler pathway, niacin forms NAD. Niacin also exhibits crosstalk with HIF and AHR cell signals in the regulation of insulin sensitivity, which is a complication in CKD. Dysregulated enzyme activity in the NAD de novo pathway increases the levels of circulating tryptophan metabolites that activate AHR, resulting in poly-ADP ribose polymerase activation, thrombosis, endothelial dysfunction, and immunosuppression. Therapeutically, metabolites from the NAD salvage pathway increase NAD production and subsequent sirtuin deacetylase activity, resulting in reduced activation of retinoic acid-inducible gene I, p53, NF-κB and SMAD2 but increased activation of FOXO1, PGC-1α, and DNA methyltransferase-1. These post-translational responses may also be initiated through non-coding RNAs (ncRNAs), which are additionally altered in CKD. Nanoparticles traverse biological systems and can penetrate almost all tissues as disease biomarkers and drug delivery carriers. Targeted delivery of non-coding RNAs or NAD metabolites with nanoparticles may enable the development of more effective diagnostics and therapies to treat CKD.
    MeSH term(s) Humans ; NAD/metabolism ; Receptors, Aryl Hydrocarbon/metabolism ; Niacin ; Signal Transduction ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Renal Insufficiency, Chronic ; Vascular Diseases ; Hypoxia ; Ischemia
    Chemical Substances NAD (0U46U6E8UK) ; Receptors, Aryl Hydrocarbon ; Niacin (2679MF687A) ; Basic Helix-Loop-Helix Transcription Factors
    Language English
    Publishing date 2023-10-09
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 2118570-0
    ISSN 1479-5876 ; 1479-5876
    ISSN (online) 1479-5876
    ISSN 1479-5876
    DOI 10.1186/s12967-023-04584-8
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  5. Article ; Online: Genetics of Focal Segmental Glomerulosclerosis in African American Children.

    Levy, Rebecca / Kopp, Jeffrey B / Franceschini, Nora

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

    2023  Volume 81, Issue 6, Page(s) 627–628

    MeSH term(s) Humans ; Child ; Glomerulosclerosis, Focal Segmental/genetics ; Black or African American/genetics ; Proteinuria
    Language English
    Publishing date 2023-04-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 604539-x
    ISSN 1523-6838 ; 0272-6386
    ISSN (online) 1523-6838
    ISSN 0272-6386
    DOI 10.1053/j.ajkd.2023.02.001
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    Zs.MO 468: Show issues

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  6. Article: Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease.

    Curran, Colleen S / Kopp, Jeffrey B

    Frontiers in pharmacology

    2022  Volume 13, Page(s) 782199

    Abstract: The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor that binds diverse endogenous and xenobiotic ligands, which regulate AHR stability, transcriptional activity, and cell signaling. AHR activity is strongly implicated ... ...

    Abstract The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix transcription factor that binds diverse endogenous and xenobiotic ligands, which regulate AHR stability, transcriptional activity, and cell signaling. AHR activity is strongly implicated throughout the course of chronic kidney disease (CKD). Many diverse organic molecules bind and activate AHR and these ligands are reported to either promote glomerular and tubular damage or protect against kidney injury. AHR crosstalk with estrogen, peroxisome proliferator-activated receptor-γ, and NF-κB pathways may contribute to the diversity of AHR responses during the various forms and stages of CKD. The roles of AHR in kidney fibrosis, metabolism and the renin angiotensin system are described to offer insight into CKD pathogenesis and therapies.
    Language English
    Publishing date 2022-02-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2022.782199
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  7. Article: RAGE pathway activation and function in chronic kidney disease and COVID-19.

    Curran, Colleen S / Kopp, Jeffrey B

    Frontiers in medicine

    2022  Volume 9, Page(s) 970423

    Abstract: The multi-ligand receptor for advanced glycation end-products (RAGE) and its ligands are contributing factors in autoimmunity, cancers, and infectious disease. RAGE activation is increased in chronic kidney disease (CKD) and coronavirus disease 2019 ( ... ...

    Abstract The multi-ligand receptor for advanced glycation end-products (RAGE) and its ligands are contributing factors in autoimmunity, cancers, and infectious disease. RAGE activation is increased in chronic kidney disease (CKD) and coronavirus disease 2019 (COVID-19). CKD may increase the risk of COVID-19 severity and may also develop in the form of long COVID. RAGE is expressed in essentially all kidney cell types. Increased production of RAGE isoforms and RAGE ligands during CKD and COVID-19 promotes RAGE activity. The downstream effects include cellular dysfunction, tissue injury, fibrosis, and inflammation, which in turn contribute to a decline in kidney function, hypertension, thrombotic disorders, and cognitive impairment. In this review, we discuss the forms and mechanisms of RAGE and RAGE ligands in the kidney and COVID-19. Because various small molecules antagonize RAGE activity in animal models, targeting RAGE, its co-receptors, or its ligands may offer novel therapeutic approaches to slowing or halting progressive kidney disease, for which current therapies are often inadequate.
    Language English
    Publishing date 2022-08-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2022.970423
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  8. Article ; Online: Impact of APOL1 kidney risk variants on glomerular transcriptomes.

    Kopp, Jeffrey B / Heymann, Jurgen

    Kidney international

    2022  Volume 102, Issue 1, Page(s) 16–19

    Abstract: McNulty and colleagues describe the glomerular transcriptional landscape of subjects with APOL1 (the gene encoding apolipoprotein L1)-associated kidney disease, using bulk RNA sequencing. They found the following: APOL1 gene expression was higher in ... ...

    Abstract McNulty and colleagues describe the glomerular transcriptional landscape of subjects with APOL1 (the gene encoding apolipoprotein L1)-associated kidney disease, using bulk RNA sequencing. They found the following: APOL1 gene expression was higher in individuals with APOL1 high-risk genetic status; in glomeruli, STC1, encoding stanniocalcin, was the most upregulated gene, and CCL18, encoding C-C motif chemokine ligand 18, was the most downregulated gene; and nuclear factor kappa BNF-κB inhibitor-interacting Ras-like 1 (NKIRAS1) is the strongest hub gene. These findings identify disease pathways that might mediate or mitigate APOL1-associated nephropathies.
    MeSH term(s) Apolipoprotein L1/genetics ; Humans ; Kidney/metabolism ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Lipoproteins, HDL/genetics ; Risk Factors ; Transcriptome
    Chemical Substances APOL1 protein, human ; Apolipoprotein L1 ; Lipoproteins, HDL
    Language English
    Publishing date 2022-06-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2022.04.019
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    Zs.A 797: Show issues Location:
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  9. Article ; Online: COVID-19-Associated Collapsing Glomerulopathy: An Emerging Entity.

    Nasr, Samih H / Kopp, Jeffrey B

    Kidney international reports

    2020  Volume 5, Issue 6, Page(s) 759–761

    Keywords covid19
    Language English
    Publishing date 2020-05-04
    Publishing country United States
    Document type Editorial ; Comment
    ISSN 2468-0249
    ISSN (online) 2468-0249
    DOI 10.1016/j.ekir.2020.04.030
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  10. Article ; Online: Global glomerulosclerosis in primary nephrotic syndrome: including age as a variable to predict renal outcomes.

    Kopp, Jeffrey B

    Kidney international

    2018  Volume 93, Issue 5, Page(s) 1043–1044

    Abstract: With normal aging, there are increased numbers of globally sclerotic glomeruli. Global glomerulosclerosis is also a feature of chronic kidney disease. In this issue, Hommos and colleagues provide data on the fraction of globally sclerotic glomeruli in ... ...

    Abstract With normal aging, there are increased numbers of globally sclerotic glomeruli. Global glomerulosclerosis is also a feature of chronic kidney disease. In this issue, Hommos and colleagues provide data on the fraction of globally sclerotic glomeruli in healthy kidney donor biopsies. This provides reference for evaluation of whether isolated global glomerulosclerosis is evidence of pathology.
    MeSH term(s) Glomerulosclerosis, Focal Segmental ; Humans ; Kidney ; Kidney Diseases ; Kidney Glomerulus ; Kidney Transplantation ; Nephrotic Syndrome
    Language English
    Publishing date 2018-04-22
    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.2018.01.020
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