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 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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Data availability
All data generated or analyzed during this study are included in this published article.
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FH designed the study, completed the experiment and supervised the data collection, JW analyzed the data, interpreted the data, FH and JW prepare the manuscript for publication and reviewed the draft of the manuscript. All authors have read and approved the manuscript.
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Author Fei Huang declares that he/she has no conflict of interest, author Jing Wei declares that he/she has no conflict of interest.
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13273_2023_371_MOESM1_ESM.jpg
Supplementary file1 MPC5 cells were treated with 30 nM glucose, UHRF1, and vector. A: Flow cytometry was used to detect cell cycle; C: Western blots showing the expression of CyclinD and CDK4; Repetition = 3. * p <0.05, *** p < 0.001 vs. HG +vector. (JPG 1748 KB)
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Huang, F., Wei, J. Knockdown of UHRF1 ameliorates high glucose-induced podocyte injury by activating SIRT4. Mol. Cell. Toxicol. (2023). https://doi.org/10.1007/s13273-023-00371-0
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DOI: https://doi.org/10.1007/s13273-023-00371-0