ArticleKidney diseases (Basel, Switzerland)2020
FGF/FGFR2 Protects against Tubular Cell Death and Acute Kidney Injury Involving Erk1/2 Signaling Activation.
Article in Kidney diseases (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- DNA hypermethylation of FGFR2 drives fibrosis in the aging kidney.Scientific reports · 2026Article
- Insulin like growth factor binding protein 7 activate JNK/ERK signaling to aggravate uranium-induced renal cell cytotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Arsenite Exposure to Human RPCs (HRTPT) Produces a Reversible Epithelial Mesenchymal Transition (EMT): In-Vitro and In-Silico Study.International journal of molecular sciences · 2023Article
- Fibroblast Growth Factor 2 Is Produced By Renal Tubular Cells to Act as a Paracrine Factor in Maladaptive Kidney Repair After Cisplatin Nephrotoxicity.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Aberrations inInternational journal of molecular sciences · 2022Article
- Roles of the fibroblast growth factor signal transduction system in tissue injury repair.Burns & trauma · 2022Review
- Role of HRTPT in kidney proximal epithelial cell regeneration: Integrative differential expression and pathway analyses using microarray and scRNA-seq.Journal of cellular and molecular medicine · 2021Article
- Role of Klotho in Hyperglycemia: Its Levels and Effects on Fibroblast Growth Factor Receptors, Glycolysis, and Glomerular Filtration.International journal of molecular sciences · 2021Article
- Circulating fibroblast growth factor-2 precipitates HIV nephropathy in mice.Disease models & mechanisms · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundFibroblast growth factors (FGFs) are heparin-binding proteins involved in a variety of biological processes, and part of them may act through binding with cell membrane receptor FGFR2.
objectivesTo clarify the role and mechanisms of FGFR2 signaling in tubular cell survival and acute kidney injury (AKI).
methodIn this study, kidney ischemia/reperfusion (IR) or cisplatin injection was used to induce AKI in mice.
resultsIn the kidneys after IR or cisplatin injection, the expression of FGFs and Erk1/2 phosphorylation were elevated. To investigate the role of FGFs in tubular cell survival and AKI, a mouse model with tubular cell specific FGFR2 gene disruption was generated. The knockouts were born normal. At 2 months of age, about one-third of the knockouts developed mild hydronephrosis. Ablation of FGFR2 in tubular cells aggravated acute kidney dysfunction as well as tubular cell apoptosis induced by IR or cisplatin. In addition, Erk1/2 phosphorylation was less in the knockout kidneys than in control littermates at day 1 after cisplatin injection. In cultured NRK-52E cells, recombinant FGF2 protein induced Erk1/2 phosphorylation and inhibited cisplatin-induced cell death. PD98059 abolished Erk1/2 phosphorylation and partly reversed the protective effect of FGF2 on cisplatin-induced cell death.
conclusionsThis study indicates that FGF/FGFR2 signaling plays an important role in protecting against tubular cell death and AKI, which is partly through stimulating Erk1/2 activation.
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