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  1. Article: Editorial for the Special Issue: Pathophysiology of Chronic Kidney Disease and Its Complications.

    Oe, Yuji

    Biomedicines

    2024  Volume 12, Issue 2

    Abstract: Chronic kidney disease (CKD) is a risk factor for end-stage kidney disease, requiring renal replacement therapy [ ... ]. ...

    Abstract Chronic kidney disease (CKD) is a risk factor for end-stage kidney disease, requiring renal replacement therapy [...].
    Language English
    Publishing date 2024-02-10
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines12020416
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  2. Article ; Online: CRRT 2023 Meeting: Targeting Amino Acid Transport to Improve Acute Kidney Injury Outcome.

    Oe, Yuji / Vallon, Volker

    Nephron

    2023  Volume 147, Issue 12, Page(s) 774–777

    Abstract: Background: In acute kidney injury (AKI), proximal tubules are a primary site of injury, resulting in significant alterations in amino acid transport and metabolism. However, little is known about the therapeutic potential of targeting amino acid ... ...

    Abstract Background: In acute kidney injury (AKI), proximal tubules are a primary site of injury, resulting in significant alterations in amino acid transport and metabolism. However, little is known about the therapeutic potential of targeting amino acid transporters. Here, we briefly review the first experimental evidence that targeting the sodium-coupled amino acid transporter SLC6A19 (B0AT1) can improve AKI outcome.
    Summary: SLC6A19 is expressed in the small intestine and early proximal tubules, where it absorbs and reabsorbs most of the ingested and filtered neutral amino acids, respectively. Systemic SLC6A19 deficiency alleviates renal cellular senescence and suppresses subsequent inflammation and fibrosis in a murine model of aristolochic acid-induced nephropathy, which targets the proximal tubule. The underlying mechanisms remain to be determined, but potentially may include reduced tubular workload, an inhibitory effect on SGLT2, downstream shift in transport and preconditioning of late proximal tubules, and induction of a fasting-like phenotype and lowering tubular accumulation of branched-chain amino acids, which all can promote tubular health.
    MeSH term(s) Humans ; Mice ; Animals ; Amino Acids/metabolism ; Kidney/metabolism ; Kidney Tubules, Proximal/metabolism ; Acute Kidney Injury/therapy ; Acute Kidney Injury/metabolism ; Amino Acid Transport Systems, Neutral
    Chemical Substances Amino Acids ; SLC6A19 protein, mouse ; Amino Acid Transport Systems, Neutral
    Language English
    Publishing date 2023-07-25
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; 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 10.1159/000531918
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  3. Article: Tissue Factor, Thrombosis, and Chronic Kidney Disease.

    Oe, Yuji / Takahashi, Nobuyuki

    Biomedicines

    2022  Volume 10, Issue 11

    Abstract: Coagulation abnormalities are common in chronic kidney disease (CKD). Tissue factor (TF, factor III) is a master regulator of the extrinsic coagulation system, activating downstream coagulation proteases, such as factor Xa and thrombin, and promoting ... ...

    Abstract Coagulation abnormalities are common in chronic kidney disease (CKD). Tissue factor (TF, factor III) is a master regulator of the extrinsic coagulation system, activating downstream coagulation proteases, such as factor Xa and thrombin, and promoting fibrin formation. TF and coagulation proteases also activate protease-activated receptors (PARs) and are implicated in various organ injuries. Recent studies have shown the mechanisms by which thrombotic tendency is increased under CKD-specific conditions. Uremic toxins, such as indoxyl sulfate and kynurenine, are accumulated in CKD and activate TF and coagulation; in addition, the TF-coagulation protease-PAR pathway enhances inflammation and fibrosis, thereby exacerbating renal injury. Herein, we review the recent research studies to understand the role of TF in increasing the thrombotic risk and CKD progression.
    Language English
    Publishing date 2022-10-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10112737
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  4. Article ; Online: Tissue Factor, Thrombosis, and Chronic Kidney Disease

    Yuji Oe / Nobuyuki Takahashi

    Biomedicines, Vol 10, Iss 2737, p

    2022  Volume 2737

    Abstract: Coagulation abnormalities are common in chronic kidney disease (CKD). Tissue factor (TF, factor III) is a master regulator of the extrinsic coagulation system, activating downstream coagulation proteases, such as factor Xa and thrombin, and promoting ... ...

    Abstract Coagulation abnormalities are common in chronic kidney disease (CKD). Tissue factor (TF, factor III) is a master regulator of the extrinsic coagulation system, activating downstream coagulation proteases, such as factor Xa and thrombin, and promoting fibrin formation. TF and coagulation proteases also activate protease-activated receptors (PARs) and are implicated in various organ injuries. Recent studies have shown the mechanisms by which thrombotic tendency is increased under CKD-specific conditions. Uremic toxins, such as indoxyl sulfate and kynurenine, are accumulated in CKD and activate TF and coagulation; in addition, the TF–coagulation protease–PAR pathway enhances inflammation and fibrosis, thereby exacerbating renal injury. Herein, we review the recent research studies to understand the role of TF in increasing the thrombotic risk and CKD progression.
    Keywords uremic toxins ; hypoxia ; coagulation ; protease-activated receptor ; Biology (General) ; QH301-705.5
    Subject code 306
    Language English
    Publishing date 2022-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
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  5. Article: The Pathophysiological Basis of Diabetic Kidney Protection by Inhibition of SGLT2 and SGLT1.

    Oe, Yuji / Vallon, Volker

    Kidney and dialysis

    2022  Volume 2, Issue 2, Page(s) 349–368

    Abstract: SGLT2 inhibitors can protect the kidneys of patients with and without type 2 diabetes mellitus and slow the progression towards end-stage kidney disease. Blocking tubular SGLT2 and spilling glucose into the urine, which triggers a metabolic counter- ... ...

    Abstract SGLT2 inhibitors can protect the kidneys of patients with and without type 2 diabetes mellitus and slow the progression towards end-stage kidney disease. Blocking tubular SGLT2 and spilling glucose into the urine, which triggers a metabolic counter-regulation similar to fasting, provides unique benefits, not only as an anti-hyperglycemic strategy. These include a low hypoglycemia risk and a shift from carbohydrate to lipid utilization and mild ketogenesis, thereby reducing body weight and providing an additional energy source. SGLT2 inhibitors counteract hyperreabsorption in the early proximal tubule, which acutely lowers glomerular pressure and filtration and thereby reduces the physical stress on the filtration barrier, the filtration of tubule-toxic compounds, and the oxygen demand for tubular reabsorption. This improves cortical oxygenation, which, together with lesser tubular gluco-toxicity and improved mitochondrial function and autophagy, can reduce pro-inflammatory, pro-senescence, and pro-fibrotic signaling and preserve tubular function and GFR in the long-term. By shifting transport downstream, SGLT2 inhibitors more equally distribute the transport burden along the nephron and may mimic systemic hypoxia to stimulate erythropoiesis, which improves oxygen delivery to the kidney and other organs. SGLT1 inhibition improves glucose homeostasis by delaying intestinal glucose absorption and by increasing the release of gastrointestinal incretins. Combined SGLT1 and SGLT2 inhibition has additive effects on renal glucose excretion and blood glucose control. SGLT1 in the macula densa senses luminal glucose, which affects glomerular hemodynamics and has implications for blood pressure control. More studies are needed to better define the therapeutic potential of SGLT1 inhibition to protect the kidney, alone or in combination with SGLT2 inhibition.
    Language English
    Publishing date 2022-06-18
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2673-8236
    ISSN 2673-8236
    DOI 10.3390/kidneydial2020032
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  6. Article: Clinical and Molecular Basis of Hepatocellular Carcinoma after Hepatitis C Virus Eradication.

    Oe, Natsumi / Takeda, Haruhiko / Eso, Yuji / Takai, Atsushi / Marusawa, Hiroyuki

    Pathogens (Basel, Switzerland)

    2022  Volume 11, Issue 4

    Abstract: Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit ... ...

    Abstract Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of direct-acting antiviral (DAA) drugs has revolutionized the treatment of HCV infection, and the vast majority of HCV patients can achieve HCV eradication using DAAs. However, mounting evidence clearly indicates that HCC inevitably occurs in a subset of patients after successful viral eradication using DAA therapy. Cancer is a genetic disease, and the accumulation of genetic and epigenetic aberrations may cause hepatocarcinogenesis in chronically damaged liver, even after virus elimination. In this review, we highlight HCC development after HCV eradication and discuss the current understanding of the molecular mechanisms of tumorigenesis after virus elimination, focusing on the genetic and epigenetic background of chronically damaged liver tissues.
    Language English
    Publishing date 2022-04-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens11040430
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  7. Article ; Online: Clinical and Molecular Basis of Hepatocellular Carcinoma after Hepatitis C Virus Eradication

    Natsumi Oe / Haruhiko Takeda / Yuji Eso / Atsushi Takai / Hiroyuki Marusawa

    Pathogens, Vol 11, Iss 430, p

    2022  Volume 430

    Abstract: Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit ... ...

    Abstract Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of direct-acting antiviral (DAA) drugs has revolutionized the treatment of HCV infection, and the vast majority of HCV patients can achieve HCV eradication using DAAs. However, mounting evidence clearly indicates that HCC inevitably occurs in a subset of patients after successful viral eradication using DAA therapy. Cancer is a genetic disease, and the accumulation of genetic and epigenetic aberrations may cause hepatocarcinogenesis in chronically damaged liver, even after virus elimination. In this review, we highlight HCC development after HCV eradication and discuss the current understanding of the molecular mechanisms of tumorigenesis after virus elimination, focusing on the genetic and epigenetic background of chronically damaged liver tissues.
    Keywords hepatitis C virus ; liver cancer ; SVR ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2022-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
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  8. Article ; Online: Coagulation, Protease-Activated Receptors, and Diabetic Kidney Disease: Lessons from eNOS-Deficient Mice.

    Oe, Yuji / Miyazaki, Mariko / Takahashi, Nobuyuki

    The Tohoku journal of experimental medicine

    2021  Volume 255, Issue 1, Page(s) 1–8

    Abstract: Endothelial nitric oxide synthase (eNOS) dysfunction is known to exacerbate the progression and prognosis of diabetic kidney disease (DKD). One of the mechanisms through which this is achieved is that low eNOS levels are associated with ... ...

    Abstract Endothelial nitric oxide synthase (eNOS) dysfunction is known to exacerbate the progression and prognosis of diabetic kidney disease (DKD). One of the mechanisms through which this is achieved is that low eNOS levels are associated with hypercoagulability, which promotes kidney injury. In the extrinsic coagulation cascade, the tissue factor (factor III) and downstream coagulation factors, such as active factor X (FXa), exacerbate inflammation through activation of the protease-activated receptors (PARs). Recently, it has been shown that the lack of or reduced eNOS expression in diabetic mice, as a model of advanced DKD, increases renal tissue factor levels and PAR1 and 2 expression in their kidneys. Furthermore, pharmaceutical inhibition or genetic deletion of coagulation factors or PARs ameliorated inflammation in DKD in mice lacking eNOS. In this review, we summarize the relationship between eNOS, coagulation, and PARs and propose a novel therapeutic option for the management of patients with DKD.
    MeSH term(s) Animals ; Antibodies, Neutralizing/administration & dosage ; Blood Coagulation ; Diabetic Nephropathies/blood ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/physiopathology ; Disease Models, Animal ; Factor Xa Inhibitors/pharmacology ; Humans ; Kidney/drug effects ; Kidney/metabolism ; Mice ; Mice, Knockout ; Nitric Oxide Synthase Type III/deficiency ; Nitric Oxide Synthase Type III/genetics ; Receptors, Proteinase-Activated/deficiency ; Receptors, Proteinase-Activated/genetics ; Receptors, Proteinase-Activated/metabolism ; Signal Transduction ; Thromboplastin/antagonists & inhibitors ; Thromboplastin/metabolism
    Chemical Substances Antibodies, Neutralizing ; Factor Xa Inhibitors ; Receptors, Proteinase-Activated ; Thromboplastin (9035-58-9) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39)
    Language English
    Publishing date 2021-08-04
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 123477-8
    ISSN 1349-3329 ; 0040-8727
    ISSN (online) 1349-3329
    ISSN 0040-8727
    DOI 10.1620/tjem.255.1
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  9. Article ; Online: Uremic toxins alter coagulation and fibrinolysis-related genes expression in human endothelial cells.

    Oe, Yuji / Sato, Emiko / Sato, Hiroshi / Miyazaki, Mariko / Ito, Sadayoshi / Takahashi, Nobuyuki

    Thrombosis research

    2019  Volume 186, Page(s) 75–77

    MeSH term(s) Blood Coagulation ; Endothelial Cells ; Fibrin Clot Lysis Time ; Fibrinolysis ; Humans ; Uremia
    Language English
    Publishing date 2019-12-26
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 121852-9
    ISSN 1879-2472 ; 0049-3848
    ISSN (online) 1879-2472
    ISSN 0049-3848
    DOI 10.1016/j.thromres.2019.12.017
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  10. Article ; Online: SGLT2 inhibitor dapagliflozin protects the kidney in a murine model of Balkan nephropathy.

    Oe, Yuji / Kim, Young Chul / Sidorenko, Viktoriya S / Zhang, Haiyan / Kanoo, Sadhana / Lopez, Natalia / Goodluck, Helen A / Crespo-Masip, Maria / Vallon, Volker

    American journal of physiology. Renal physiology

    2023  Volume 326, Issue 2, Page(s) F227–F240

    Abstract: Proximal tubular uptake of aristolochic acid (AA) forms aristolactam (AL)-DNA adducts, which cause a p53/p21-mediated DNA damage response and acute tubular injury. Recurrent AA exposure causes kidney function loss and fibrosis in humans (Balkan endemic ... ...

    Abstract Proximal tubular uptake of aristolochic acid (AA) forms aristolactam (AL)-DNA adducts, which cause a p53/p21-mediated DNA damage response and acute tubular injury. Recurrent AA exposure causes kidney function loss and fibrosis in humans (Balkan endemic nephropathy) and mice and is a model of (acute kidney injury) AKI to chronic kidney disease (CKD) transition. Inhibitors of the proximal tubule sodium-glucose transporter SGLT2 can protect against CKD progression, but their effect on AA-induced kidney injury remains unknown. C57BL/6J mice (15-wk-old) were administered vehicle or AA every 3 days for 3 wk (10 and 3 mg/kg ip in females and males, respectively). Dapagliflozin (dapa, 0.01 g/kg diet) or vehicle was initiated 7 days prior to AA injections. All dapa effects were sex independent, including a robust glycosuria. Dapa lowered urinary kidney-injury molecule 1 (KIM-1) and albumin (both normalized to creatinine) after the last AA injection and kidney mRNA expression of early DNA damage response markers (
    MeSH term(s) Humans ; Male ; Female ; Mice ; Animals ; Balkan Nephropathy/metabolism ; Balkan Nephropathy/pathology ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2/metabolism ; Disease Models, Animal ; Creatinine/metabolism ; Tumor Suppressor Protein p53/metabolism ; Mice, Inbred C57BL ; Kidney/metabolism ; Aristolochic Acids/toxicity ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/prevention & control ; Renal Insufficiency, Chronic/metabolism ; Fibrosis ; Glucose Transport Proteins, Facilitative/metabolism ; Sodium/metabolism ; Benzhydryl Compounds ; Glucosides
    Chemical Substances aristolochic acid I (94218WFP5T) ; Sodium-Glucose Transporter 2 Inhibitors ; dapagliflozin (1ULL0QJ8UC) ; Sodium-Glucose Transporter 2 ; Creatinine (AYI8EX34EU) ; Tumor Suppressor Protein p53 ; Aristolochic Acids ; Glucose Transport Proteins, Facilitative ; Sodium (9NEZ333N27) ; Benzhydryl Compounds ; Glucosides
    Language English
    Publishing date 2023-11-30
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; 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.00228.2023
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