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      KCI등재 SCIE SCOPUS

      Knockdown of UHRF1 ameliorates high glucose-induced podocyte injury by activating SIRT4

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      https://www.riss.kr/link?id=A109136710

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      다국어 초록 (Multilingual Abstract)

      Backgrounds Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and current treatment options to prevent its progression are inadequate. Podocyte injury is crucial to the pathogenesis of DN. Objective This study aimed to inves...

      Backgrounds Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and current treatment options to prevent its progression are inadequate. Podocyte injury is crucial to the pathogenesis of DN.


      Objective This study aimed to investigate the effect of UHRF1 on high glucose (HG)-induced podocyte injury and to explore its molecular mechanism.


      Results HG induced MPC5 cells to highly express UHRF1 while downregulating SIRT4. Knockdown of UHRF1 promoted HG-induced proliferation of MPC5 cells and ameliorated HG-induced cell cycle arrest, apoptosis, and ROS levels. Knockdown of UHRF1 ameliorated HG-induced podocyte injury by upregulating SIRT4.


      Conclusions Knockdown of UHRF1 ameliorates HG-induced podocyte injury by upregulating SIRT4, indicating that UHRF1 may be a novel target for preventing DN in podocytes.

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      다국어 초록 (Multilingual Abstract)

      Backgrounds Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and current treatment options to prevent its progression are inadequate. Podocyte injury is crucial to the pathogenesis of DN. Objective This study aimed to inv...

      Backgrounds Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and current treatment options to prevent its progression are inadequate. Podocyte injury is crucial to the pathogenesis of DN.




      Objective This study aimed to investigate the effect of UHRF1 on high glucose (HG)-induced podocyte injury and to explore its molecular mechanism.




      Results HG induced MPC5 cells to highly express UHRF1 while downregulating SIRT4. Knockdown of UHRF1 promoted HG-induced proliferation of MPC5 cells and ameliorated HG-induced cell cycle arrest, apoptosis, and ROS levels. Knockdown of UHRF1 ameliorated HG-induced podocyte injury by upregulating SIRT4.




      Conclusions Knockdown of UHRF1 ameliorates HG-induced podocyte injury by upregulating SIRT4, indicating that UHRF1 may be a novel target for preventing DN in podocytes.

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