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  1. Article: Constitutive Plasma Membrane Turnover in T-REx293 cells via Ordered Membrane Domain Endocytosis under Mitochondrial Control.

    Deisl, Christine / Moe, Orson W / Hilgemann, Donald W

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Clathrin/dynamin-independent endocytosis of ordered plasma membrane domains ( ...

    Abstract Clathrin/dynamin-independent endocytosis of ordered plasma membrane domains (
    Language English
    Publishing date 2024-02-14
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.17.576124
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  2. Article ; Online: A generic crystallopathic model for chronic kidney disease progression.

    Moe, Orson W

    The Journal of clinical investigation

    2021  Volume 131, Issue 16

    Abstract: Chronic kidney disease (CKD) has reached epidemic proportions globally. The natural course of chronic kidney disease is almost uniformly progressive, albeit at different rates in different individuals. The downhill course appears to pervade kidney ... ...

    Abstract Chronic kidney disease (CKD) has reached epidemic proportions globally. The natural course of chronic kidney disease is almost uniformly progressive, albeit at different rates in different individuals. The downhill course appears to pervade kidney diseases of all etiologies and seems to spiral down a self-perpetuating vortex, even if the original insult is ameliorated or controlled. In this issue of the JCI, Shiizaki, Tsubouchi, and colleagues proposed a model of renal tubule luminal calcium phosphate crystallopathy that accounts for renal function demise. Calcium phosphate crystals attached to TLR4 and underwent endocytosis at the brush border, triggering inflammation and fibrosis. This mechanism might operate in different kinds of kidney disease, with a theoretical phosphate concentration threshold in the proximal tubular lumen, beyond which is triggered undesirable downstream effects that eventuate in loss of renal function. If this model parallels human CKD, clinicians may focus efforts on determining phosphate exposure in the proximal tubular lumen.
    MeSH term(s) Fibrosis ; Humans ; Inflammation ; Kidney Tubules ; Phosphates ; Renal Insufficiency, Chronic
    Chemical Substances Phosphates
    Language English
    Publishing date 2021-08-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI151858
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    Ua VI Zs.184: Show issues Location:
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  3. Article ; Online: Uric acid transport, transporters, and their pharmacological targeting.

    Adomako, Emmanuel A / Moe, Orson W

    Acta physiologica (Oxford, England)

    2023  Volume 238, Issue 2, Page(s) e13980

    Abstract: Knowledge of uric acid (UA) crystallopathies preceded the identification of this compound. How the body handles and transports UA proved even more elusive. Over several decades, advances in molecular phenotyping have illuminated this hitherto nebulous ... ...

    Abstract Knowledge of uric acid (UA) crystallopathies preceded the identification of this compound. How the body handles and transports UA proved even more elusive. Over several decades, advances in molecular phenotyping have illuminated this hitherto nebulous field. Closely parallel to the characterization of the transport mechanisms of UA in the body was the development of drugs designed to manipulate UA levels. In this review, we highlight the study of UA transport and transporters. This is an evolving field, and we expect our knowledge of the transport mechanisms to both widen and deepen further. We focus on the best-characterized transporters rather than an exhaustive catalog of all suspected transporters. We review the established and novel compounds that modulate UA transport.
    MeSH term(s) Uric Acid ; Membrane Transport Proteins ; Glucose Transport Proteins, Facilitative
    Chemical Substances Uric Acid (268B43MJ25) ; Membrane Transport Proteins ; Glucose Transport Proteins, Facilitative
    Language English
    Publishing date 2023-05-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13980
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  4. Article ; Online: The Effects of Acid on Calcium and Phosphate Metabolism.

    Salcedo-Betancourt, Juan D / Moe, Orson W

    International journal of molecular sciences

    2024  Volume 25, Issue 4

    Abstract: A variety of changes in mineral metabolism aiming to restore acid-base balance occur in acid loading and metabolic acidosis. Phosphate plays a key role in defense against metabolic acidosis, both as an intracellular and extracellular buffer, as well as ... ...

    Abstract A variety of changes in mineral metabolism aiming to restore acid-base balance occur in acid loading and metabolic acidosis. Phosphate plays a key role in defense against metabolic acidosis, both as an intracellular and extracellular buffer, as well as in the renal excretion of excess acid in the form of urinary titratable acid. The skeleton acts as an extracellular buffer in states of metabolic acidosis, as the bone matrix demineralizes, leading to bone apatite dissolution and the release of phosphate, calcium, carbonate, and citrate into the circulation. The renal handling of calcium, phosphate and citrate is also affected, with resultant hypercalciuria, hyperphosphaturia and hypocitraturia.
    MeSH term(s) Humans ; Calcium/metabolism ; Kidney/metabolism ; Acidosis/metabolism ; Citric Acid ; Kidney Diseases ; Citrates ; Calcium, Dietary ; Phosphates/metabolism
    Chemical Substances Calcium (SY7Q814VUP) ; Citric Acid (2968PHW8QP) ; Citrates ; Calcium, Dietary ; Phosphates
    Language English
    Publishing date 2024-02-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25042081
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  5. Article ; Online: Bone Dysregulation in Acute Kidney Injury.

    Neyra, Javier A / Moe, Orson W

    Nephron

    2023  Volume 147, Issue 12, Page(s) 747–753

    Abstract: Acute kidney injury (AKI) is a highly prevalent condition with multiple acute and chronic consequences. Survivors of AKI are at risk of AKI-to-chronic kidney disease (CKD) transition, which carries significant morbidity and mortality. One retrospective ... ...

    Abstract Acute kidney injury (AKI) is a highly prevalent condition with multiple acute and chronic consequences. Survivors of AKI are at risk of AKI-to-chronic kidney disease (CKD) transition, which carries significant morbidity and mortality. One retrospective analysis showed increased risk of bone fracture post-AKI in humans, which was independent of CKD development. While there are several theoretical reasons for late disturbances of bone health post-AKI, no definitive data are available to date. An important question is whether there are bone sequelae from AKI that are independent of CKD, meaning bone disease prior to the onset, or in the absence of CKD - a form of "post-AKI osteopathy." While preclinical studies examining bone health after acute stressors have focused mostly on sepsis models, multiple experimental AKI models are readily available for longitudinal bone health interrogation. Future research should be tailored to define whether AKI is a risk factor, independent of CKD, for bone disease and if present, the time course and type of bone disease. This review summarizes a fraction of the existing data to provide some guidance in future research efforts.
    MeSH term(s) Humans ; Retrospective Studies ; Acute Kidney Injury/complications ; Renal Insufficiency, Chronic/complications ; Risk Factors ; Bone Diseases/complications
    Language English
    Publishing date 2023-09-27
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 207121-6
    ISSN 2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
    ISSN (online) 2235-3186 ; 1423-0186
    ISSN 1660-8151 ; 0028-2766
    DOI 10.1159/000534228
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 169: Show issues Location:
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  6. Article ; Online: 'Reviving' the call for standardization of the composite outcome of major adverse kidney events in critical care nephrology research.

    Flannery, Alexander H / Woodward, Blake M / Barreto, Erin F / Moe, Orson W / Neyra, Javier A

    Intensive care medicine

    2024  

    Language English
    Publishing date 2024-04-15
    Publishing country United States
    Document type Letter
    ZDB-ID 80387-x
    ISSN 1432-1238 ; 0340-0964 ; 0342-4642 ; 0935-1701
    ISSN (online) 1432-1238
    ISSN 0340-0964 ; 0342-4642 ; 0935-1701
    DOI 10.1007/s00134-024-07429-0
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    Zs.A 1089: Show issues Location:
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  7. Article: Phosphate and Cellular Senescence.

    Hu, Ming Chang / Moe, Orson W

    Advances in experimental medicine and biology

    2022  Volume 1362, Page(s) 55–72

    Abstract: Cellular senescence is one type of permeant arrest of cell growth and one of increasingly recognized contributor to aging and age-associated disease. High phosphate and low Klotho individually and synergistically lead to age-related degeneration in ... ...

    Abstract Cellular senescence is one type of permeant arrest of cell growth and one of increasingly recognized contributor to aging and age-associated disease. High phosphate and low Klotho individually and synergistically lead to age-related degeneration in multiple organs. Substantial evidence supports the causality of high phosphate in cellular senescence, and potential contribution to human aging, cancer, cardiovascular, kidney, neurodegenerative, and musculoskeletal diseases. Phosphate can induce cellular senescence both by direct phosphotoxicity, and indirectly through downregulation of Klotho and upregulation of plasminogen activator inhibitor-1. Restriction of dietary phosphate intake and blockage of intestinal absorption of phosphate help suppress cellular senescence. Supplementation of Klotho protein, cellular senescence inhibitor, and removal of senescent cells with senolytic agents are potential novel strategies to attenuate phosphate-induced cellular senescence, retard aging, and ameliorate age-associated, and phosphate-induced disorders.
    MeSH term(s) Aging/metabolism ; Cellular Senescence/physiology ; Down-Regulation ; Humans ; Phosphates/metabolism ; Up-Regulation
    Chemical Substances Phosphates
    Language English
    Publishing date 2022-03-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 410187-X
    ISSN 0065-2598
    ISSN 0065-2598
    DOI 10.1007/978-3-030-91623-7_7
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    Zs.A 3192: Show issues Location:
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    Einzelsignatur: Show issues

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  8. Article ; Online: Strategies to lower fibroblast growth factor 23 bioactivity.

    Verbueken, Devin / Moe, Orson W

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

    2021  Volume 37, Issue 10, Page(s) 1800–1807

    Abstract: Fibroblast growth factor 23 (FGF23) is a circulating hormone derived from the bone whose release is controlled by many factors and exerts a multitude of systemic actions. There are congenital and acquired disorders of increased and decreased FGF23 levels. ...

    Abstract Fibroblast growth factor 23 (FGF23) is a circulating hormone derived from the bone whose release is controlled by many factors and exerts a multitude of systemic actions. There are congenital and acquired disorders of increased and decreased FGF23 levels. In chronic kidney disease (CKD), elevations of FGF23 levels can be 1000-fold above the upper physiological limit. It is still debated whether this high FGF23 in CKD is a biomarker or causally related to morbidity and mortality. Data from human association studies support pathogenicity, while experimental data are less robust. Knowledge of the biology and pathobiology of FGF23 has generated a plethora of means to reduce FGF23 bioactivity at many levels that will be useful for therapeutic translations. This article summarizes these approaches and addresses several critical questions that still need to be answered.
    MeSH term(s) Biomarkers ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/metabolism ; Glucuronidase/physiology ; Hormones ; Humans ; Renal Insufficiency, Chronic/metabolism
    Chemical Substances Biomarkers ; Hormones ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31)
    Language English
    Publishing date 2021-01-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 90594-x
    ISSN 1460-2385 ; 0931-0509
    ISSN (online) 1460-2385
    ISSN 0931-0509
    DOI 10.1093/ndt/gfab012
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    Zs.A 2198: Show issues Location:
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    Zs.MO 329: Show issues

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  9. Article ; Online: Uric Acid and Urate in Urolithiasis: The Innocent Bystander, Instigator, and Perpetrator.

    Adomako, Emmanuel / Moe, Orson W

    Seminars in nephrology

    2021  Volume 40, Issue 6, Page(s) 564–573

    Abstract: Uric acid is an end product of purine metabolism in human beings. An unusual and still unexplained phenomenon is that higher primates have relatively high uric acid levels in body fluids owing to a combination of absence of degradation and renal ... ...

    Abstract Uric acid is an end product of purine metabolism in human beings. An unusual and still unexplained phenomenon is that higher primates have relatively high uric acid levels in body fluids owing to a combination of absence of degradation and renal retention. The physiologic purpose of high uric acid levels still is enigmatic, but the pathobiologic burden is a variety of crystallopathies owing to the low aqueous solubility of uric acid such as gouty arthritis and acute uric acid nephropathy. In the urinary space, three distinct conditions result from chronic uric acid and/or urate precipitation. The first and most common variety is uric acid urolithiasis. In this condition, urate is a victim of a systemic metabolic disease in which increased acid load to the kidney is coupled with diminished urinary buffer capacity owing to defective ammonium excretion, resulting in titration of urate to its sparingly soluble protonated counterpart, uric acid, and the formation of stones. Uric acid is the innocent bystander of the crime. The second variety is hyperuricosuric calcium urolithiasis, in which uric acid confers lithogenicity via promotion of calcium oxalate precipitation by multiple mechanisms involving soluble, colloidal, and crystalline urate salts. Uric acid is the instigator of the crime. The third and least common condition involves urate as an integral part of the urolith as an ammonium salt driven by high ammonium and high urate concentrations in urine. Here, uric acid is one of the perpetrators of the crime. Both known and postulated pathogenesis of these three types of urolithiasis are reviewed and summarized.
    MeSH term(s) Animals ; Calcium Oxalate ; Humans ; Kidney Diseases ; Uric Acid ; Urinary Calculi ; Urolithiasis/etiology
    Chemical Substances Calcium Oxalate (2612HC57YE) ; Uric Acid (268B43MJ25)
    Language English
    Publishing date 2021-03-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604652-6
    ISSN 1558-4488 ; 0270-9295
    ISSN (online) 1558-4488
    ISSN 0270-9295
    DOI 10.1016/j.semnephrol.2020.12.003
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    Se 784: Show issues Location:
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  10. Article ; Online: Urine pH and Citrate as Predictors of Calcium Phosphate Stone Formation.

    Adomako, Emmanuel A / Li, Xilong / Sakhaee, Khashayar / Moe, Orson W / Maalouf, Naim M

    Kidney360

    2023  Volume 4, Issue 8, Page(s) 1123–1129

    MeSH term(s) Citric Acid ; Phosphates ; Citrates ; Calcium Phosphates ; Hydrogen-Ion Concentration
    Chemical Substances Citric Acid (2968PHW8QP) ; Phosphates ; Citrates ; calcium phosphate (97Z1WI3NDX) ; Calcium Phosphates
    Language English
    Publishing date 2023-06-12
    Publishing country United States
    Document type Journal Article
    ISSN 2641-7650
    ISSN (online) 2641-7650
    DOI 10.34067/KID.0000000000000184
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