ArticleMolecular medicine reports2018
Overexpression of KLF5 inhibits puromycin‑induced apoptosis of podocytes.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Icariin ameliorates minimal change disease by regulating the mitochondrial dysfunction pathway: an integrated strategy of network pharmacology, bioinformatics, and experimental validation.Frontiers in pharmacology · 2025Article
- Depression of LncRNA DANCR alleviates tubular injury in diabetic nephropathy by regulating KLF5 through sponge miR-214-5p.BMC nephrology · 2024Article
- Dapagliflozin improves podocytes injury in diabetic nephropathy via regulating cholesterol balance through KLF5 targeting the ABCA1 signalling pathway.Diabetology & metabolic syndrome · 2024Article
- The miR-143/145 cluster induced by TGF-β1 suppresses Wilms' tumor 1 expression in cultured human podocytes.American journal of physiology. Renal physiology · 2023Article
- The protective effects of butorphanol tartrate against homocysteine-induced blood-brain barrier dysfunction.Bioengineered · 2022Article
- Renoprotective Effect of KLF2 on Glomerular Endothelial Dysfunction in Hypertensive Nephropathy.Cells · 2022Article
- Investigating the Molecular Mechanism of Quercetin Protecting against Podocyte Injury to Attenuate Diabetic Nephropathy through Network Pharmacology, MicroarrayData Analysis, and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Recent Advances in Diabetic Kidney Diseases: From Kidney Injury to Kidney Fibrosis.International journal of molecular sciences · 2021Review
- Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 2021Review
- Transcription factor Kruppel-like factor 5 positively regulates the expression of AarF domain containing kinase 4.Molecular biology reports · 2020Article
- Krupple-Like Factor 5 is a Potential Therapeutic Target and Prognostic Marker in Epithelial Ovarian Cancer.Frontiers in pharmacology · 2020Article
- MicroRNA-21 promotes proliferation in acute myeloid leukemia by targeting Krüppel-like factor 5.Oncology letters · 2019Article
- Krϋppel-like factors (KLFs) in renal physiology and disease.EBioMedicine · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the most common microvascular complications associated with diabetes mellitus (DM); the incidence has been predicted to reach 7.7% by 2030 on a global scale. Krüppel‑like factor 5 (KLF5) is involved in numerous important biological processes; however, the potential effects of KLF5 on podocytes in patients with diabetic nephrotic (DN) have not yet been investigated. In the present study, synaptopodin expression in podocytes was investigated using an immunofluorescence assay. Following this, the proliferation of podocytes was investigated using an MTT assay. In addition, KLF5 was overexpressed in podocytes, and cell cycle arrest and apoptosis was subsequently investigated using flow cytometry. Western blotting and reverse transcription‑quantitative polymerase chain reaction assays were performed to detect the expression levels of genes involved in the cell cycle and apoptosis, and the extracellular signal‑regulated protein kinase (ERK)/p38 mitogen‑activated protein (MAP) kinase pathway. The results demonstrated that treatment with puromycin aminonucleoside (PAN) suppressed the proliferation of podocytes in a dose‑ and time‑dependent manner, and overexpression of KLF5 induced cell cycle arrest of podocytes regulated by PAN. Furthermore, overexpression of KLF5 was revealed to have inhibited PAN‑induced apoptosis of podocytes, and that overexpression of KLF5 suppressed the ERK/p38 MAP kinase pathway in podocytes induced by PAN. Therefore, the results of the present study suggested that KLF5 may represent a potential therapeutic target for treatment of patients with DN.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.