ArticleAmerican journal of physiology. Renal physiology2013
EGFR activity is required for renal tubular cell dedifferentiation and proliferation in a murine model of folic acid-induced acute kidney injury.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 63 citations in OpenAlex.
- Uromodulin alleviates fibrosis in acute kidney injury to chronic kidney disease transition by reducing EGFR.Cell communication and signaling : CCS · 2025Article
- Targeting the epidermal growth factor receptor (EGFR/ErbB) for the potential treatment of renal pathologies.Frontiers in pharmacology · 2024Review
- Pharmacological inhibition of the mixed lineage leukemia 1-menin interaction aggravates acute kidney injury induced by folic acid and ischemia-reperfusion in mice.American journal of physiology. Renal physiology · 2023Article
- NAC Pre-Administration Prevents Cardiac Mitochondrial Bioenergetics, Dynamics, Biogenesis, and Redox Alteration in Folic Acid-AKI-Induced Cardio-Renal Syndrome Type 3.Antioxidants (Basel, Switzerland) · 2023Article
- Biliary epithelial cells are facultative liver stem cells during liver regeneration in adult zebrafish.JCI insight · 2023Article
- Persistent DNA damage underlies tubular cell polyploidization and progression to chronic kidney disease in kidneys deficient in the DNA repair protein FAN1.Kidney international · 2022Article
- Tenovin-1 Ameliorates Renal Fibrosis in High-Fat-Diet-Induced Diabetic Nephropathy via Antioxidant and Anti-Inflammatory Pathways.Antioxidants (Basel, Switzerland) · 2022Article
- Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease.International journal of molecular sciences · 2022Review
- Review
- Nanobodies: new avenue to treat kidney disease.Cell and tissue research · 2021Review
- Xiaoyu Xiezhuo Drink Protects against Ischemia-Reperfusion Acute Kidney Injury in Aged Mice through Inhibiting the TGF-BioMed research international · 2021Article
- Cathelicidin-related antimicrobial peptide protects against ischaemia reperfusion-induced acute kidney injury in mice.British journal of pharmacology · 2020Article
- FGF/FGFR2 Protects against Tubular Cell Death and Acute Kidney Injury Involving Erk1/2 Signaling Activation.Kidney diseases (Basel, Switzerland) · 2020Article
- Potential targeted therapy and diagnosis based on novel insight into growth factors, receptors, and downstream effectors in acute kidney injury and acute kidney injury-chronic kidney disease progression.Signal transduction and targeted therapy · 2020Review
- Renal Inflammation and Fibrosis: A Double-edged Sword.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- Enhancing regeneration after acute kidney injury by promoting cellular dedifferentiation in zebrafish.Disease models & mechanisms · 2019Article
- EGFR drives the progression of AKI to CKD through HIPK2 overexpression.Theranostics · 2019Article
- Multiparametric MRI detects longitudinal evolution of folic acid-induced nephropathy in mice.American journal of physiology. Renal physiology · 2018Article
- EGF Receptor-Dependent YAP Activation Is Important for Renal Recovery from AKI.Journal of the American Society of Nephrology : JASN · 2018Article
- Inflammation and renal fibrosis: Recent developments on key signaling molecules as potential therapeutic targets.European journal of pharmacology · 2018Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Proliferation of dedifferentiated intrinsic renal tubular cells has been recognized to be the major cellular event that contributes to renal repair after acute kidney injury (AKI). However, the underlying mechanism that initiates renal tubular dedifferentiation in vivo remains unexplored. Here we investigated whether epidermal growth factor receptor (EGFR) mediates this process in a murine model of folic acid (FA)-induced AKI using waved-2 mice that have reduced tyrosine kinase activity of EGFR and gefitinib, a specific EGFR inhibitor. Administration of FA for 48 h induced EGFR phosphorylation in the kidney of wild-type mice, but this was inhibited in waved-2 mice and wild-type mice given gefitinib. Compared with wild-type mice, waved-2 mice and wild-type mice treated with gefitinib had increased renal dysfunction, histologic damage, and tubular cell apoptosis after FA administration. PAX2, a dedifferentiation marker, and proliferating cell nuclear antigen, a proliferating marker, were highly expressed in renal tubular cells in wild-type mice; however, their expression was largely inhibited in the kidney of waved-2 mice. Inhibition of EGFR with gefitinib also blocked FA-induced expression of these two proteins in wild-type mice. Moreover, FA exposure resulted in phosphorylation of AKT, a downstream signaling molecule of the phosphatidylinositol 3-kinases pathway associated with renal epithelial proliferation in wild-type mice, and its phosphorylation was totally suppressed in waved-2 mice and wild-type mice given gefitinib. Taken together, these results suggest that EGFR activation is essential for initiation of renal tubular cell dedifferentiation and proliferation after AKI.
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