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  1. Artikel ; Online: Podocyte Ercc1 is indispensable for glomerular integrity.

    Hama, Eriko Yoshida / Nakamichi, Ran / Hishikawa, Akihito / Kihara, Miho / Abe, Takaya / Yoshimoto, Norifumi / Nishimura, Erina Sugita / Itoh, Hiroshi / Hayashi, Kaori

    Biochemical and biophysical research communications

    2024  Band 704, Seite(n) 149713

    Abstract: As life expectancy continues to increase, age-related kidney diseases are becoming more prevalent. Chronic kidney disease (CKD) is not only a consequence of aging but also a potential accelerator of aging process. Here we report the pivotal role of ... ...

    Abstract As life expectancy continues to increase, age-related kidney diseases are becoming more prevalent. Chronic kidney disease (CKD) is not only a consequence of aging but also a potential accelerator of aging process. Here we report the pivotal role of podocyte ERCC1, a DNA repair factor, in maintaining glomerular integrity and a potential effect on multiple organs. Podocyte-specific ERCC1-knockout mice developed severe proteinuria, glomerulosclerosis, and renal failure, accompanied by a significant increase in glomerular DNA single-strand breaks (SSBs) and double-strand breaks (DSBs). ERCC1 gene transfer experiment in the knockout mice attenuated proteinuria and glomerulosclerosis with reduced DNA damage. Notably, CD44
    Mesh-Begriff(e) Humans ; Mice ; Animals ; Podocytes/metabolism ; Kidney Glomerulus/metabolism ; Kidney Diseases/metabolism ; Mice, Knockout ; Proteinuria/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Endonucleases/genetics ; Endonucleases/metabolism
    Chemische Substanzen Ercc1 protein, mouse (EC 3.1.-) ; DNA-Binding Proteins ; Endonucleases (EC 3.1.-)
    Sprache Englisch
    Erscheinungsdatum 2024-02-23
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2024.149713
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Predicting exacerbation of renal function by DNA methylation clock and DNA damage of urinary shedding cells: a pilot study.

    Hishikawa, Akihito / Nishimura, Erina Sugita / Yoshimoto, Norifumi / Nakamichi, Ran / Hama, Eriko Yoshida / Ito, Wataru / Maruki, Tomomi / Nagashima, Kengo / Shimizu-Hirota, Ryoko / Takaishi, Hiromasa / Itoh, Hiroshi / Hayashi, Kaori

    Scientific reports

    2024  Band 14, Heft 1, Seite(n) 11530

    Abstract: Recent reports have shown the feasibility of measuring biological age from DNA methylation levels in blood cells from specific regions identified by machine learning, collectively known as the epigenetic clock or DNA methylation clock. While extensive ... ...

    Abstract Recent reports have shown the feasibility of measuring biological age from DNA methylation levels in blood cells from specific regions identified by machine learning, collectively known as the epigenetic clock or DNA methylation clock. While extensive research has explored the association of the DNA methylation clock with cardiovascular diseases, cancer, and Alzheimer's disease, its relationship with kidney diseases remains largely unexplored. In particular, it is unclear whether the DNA methylation clock could serve as a predictor of worsening kidney function. In this pilot study involving 20 subjects, we investigated the association between the DNA methylation clock and subsequent deterioration of renal function. Additionally, we noninvasively evaluated DNA damage in urinary shedding cells using a previously reported method to examine the correlation with the DNA methylation clock and worsening kidney function. Our findings revealed that patients with an accelerated DNA methylation clock exhibited increased DNA damage in urinary shedding cells, along with a higher rate of eGFR decline. Moreover, in cases of advanced CKD (G4-5), the DNA damage in urinary shedding cells was significantly increased, highlighting the interplay between elevated DNA damage and eGFR decline. This study suggests the potential role of the DNA methylation clock and urinary DNA damage as predictive markers for the progression of chronic kidney disease.
    Mesh-Begriff(e) Humans ; DNA Methylation ; Pilot Projects ; Male ; DNA Damage ; Female ; Middle Aged ; Aged ; Renal Insufficiency, Chronic/urine ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/pathology ; Glomerular Filtration Rate ; Disease Progression ; Biomarkers/urine ; Kidney/metabolism ; Kidney/pathology ; Epigenesis, Genetic
    Sprache Englisch
    Erscheinungsdatum 2024-05-21
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-024-62405-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: DNA-damaged podocyte-CD8 T cell crosstalk exacerbates kidney injury by altering DNA methylation.

    Nakamichi, Ran / Hishikawa, Akihito / Chikuma, Shunsuke / Yoshimura, Akihiko / Sasaki, Takashi / Hashiguchi, Akinori / Abe, Takaya / Tokuhara, Tomoko / Yoshimoto, Norifumi / Nishimura, Erina Sugita / Hama, Eriko Yoshida / Azegami, Tatsuhiko / Nakayama, Takashin / Hayashi, Kaori / Itoh, Hiroshi

    Cell reports

    2023  Band 42, Heft 4, Seite(n) 112302

    Abstract: Recent epigenome-wide studies suggest an association between blood DNA methylation and kidney function. However, the pathological importance remains unclear. Here, we show that the homing endonuclease I-PpoI-induced DNA double-strand breaks in kidney ... ...

    Abstract Recent epigenome-wide studies suggest an association between blood DNA methylation and kidney function. However, the pathological importance remains unclear. Here, we show that the homing endonuclease I-PpoI-induced DNA double-strand breaks in kidney glomerular podocytes cause proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis with DNA methylation changes in blood cells as well as in podocytes. Single-cell RNA-sequencing analysis reveals an increase in cytotoxic CD8
    Mesh-Begriff(e) Humans ; Podocytes/metabolism ; DNA Methylation/genetics ; CD8-Positive T-Lymphocytes/metabolism ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; Kidney/metabolism ; Proteinuria/genetics ; Proteinuria/metabolism ; Proteinuria/pathology ; Renal Insufficiency, Chronic/pathology ; DNA Damage ; DNA/metabolism
    Chemische Substanzen NK Cell Lectin-Like Receptor Subfamily K ; DNA (9007-49-2)
    Sprache Englisch
    Erscheinungsdatum 2023-03-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112302
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: DNA-damaged podocyte-CD8 T cell crosstalk exacerbates kidney injury by altering DNA methylation.

    Nakamichi, Ran / Hishikawa, Akihito / Chikuma, Shunsuke / Yoshimura, Akihiko / Sasaki, Takashi / Hashiguchi, Akinori / Abe, Takaya / Tokuhara, Tomoko / Yoshimoto, Norifumi / Nishimura, Erina Sugita / Hama, Eriko Yoshida / Azegami, Tatsuhiko / Nakayama, Takashin / Hayashi, Kaori / Itoh, Hiroshi

    Cell reports

    2023  Band 42, Heft 5, Seite(n) 112427

    Sprache Englisch
    Erscheinungsdatum 2023-04-19
    Erscheinungsland United States
    Dokumenttyp Published Erratum
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112427
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Clinical significance of serum urea-to-creatinine ratio in patients undergoing peritoneal dialysis.

    Tonomura, Shun / Uchiyama, Kiyotaka / Nakayama, Takashin / Mitsuno, Ryunosuke / Kojima, Daiki / Hama, Eriko Yoshida / Nagasaka, Tomoki / Nishimura, Erina Sugita / Kusahana, Ei / Takahashi, Rina / Yoshimoto, Norifumi / Yamaguchi, Shintaro / Morimoto, Kohkichi / Yoshida, Tadashi / Hayashi, Kaori / Kanda, Takeshi / Washida, Naoki / Itoh, Hiroshi

    Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy

    2023  Band 27, Heft 6, Seite(n) 1103–1112

    Abstract: Introduction: We aimed to determine the correlation between the serum urea-to-creatinine ratio and residual kidney function (RKF) in patients undergoing peritoneal dialysis (PD), as well as its predictive value for PD-related outcomes.: Methods: This ...

    Abstract Introduction: We aimed to determine the correlation between the serum urea-to-creatinine ratio and residual kidney function (RKF) in patients undergoing peritoneal dialysis (PD), as well as its predictive value for PD-related outcomes.
    Methods: This study included a cross-sectional study to assess the correlation between serum urea-to-creatinine ratio and RKF in 50 patients on PD and a retrospective cohort study to assess the association between serum urea-to-creatinine ratio and PD-related outcomes in 122 patients who initiated PD.
    Results: Serum urea-to-creatinine ratios had significant positive correlations with renal Kt/V and creatinine clearance values (r = 0.60, p < 0.001 and r = 0.61, p < 0.001, respectively). Additionally, serum urea-to-creatinine ratio was significantly associated with a lower risk of transfer to hemodialysis or PD/hemodialysis hybrid therapy (hazard ratio: 0.84, 95% confidence interval: 0.75-0.95).
    Conclusion: The serum urea-to-creatinine ratio can be an indicator of RKF and a prognostic factor in patients undergoing PD.
    Mesh-Begriff(e) Humans ; Creatinine ; Kidney Failure, Chronic/therapy ; Retrospective Studies ; Clinical Relevance ; Cross-Sectional Studies ; Peritoneal Dialysis ; Urea
    Chemische Substanzen Creatinine (AYI8EX34EU) ; Urea (8W8T17847W)
    Sprache Englisch
    Erscheinungsdatum 2023-06-22
    Erscheinungsland Australia
    Dokumenttyp Journal Article
    ZDB-ID 2119809-3
    ISSN 1744-9987 ; 1091-6660 ; 1744-9979
    ISSN (online) 1744-9987
    ISSN 1091-6660 ; 1744-9979
    DOI 10.1111/1744-9987.14030
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

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