ArticleCell death & disease2017
FGFR1 is critical for the anti-endothelial mesenchymal transition effect of N-acetyl-seryl-aspartyl-lysyl-proline via induction of the MAP4K4 pathway.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 72 citations in OpenAlex.
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- Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease.Science advances · 2024Article
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- Plasma NOTCH3 and the risk of cardiovascular recurrence in patients with ischemic stroke.QJM : monthly journal of the Association of Physicians · 2024Article
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- Drugs for Diabetes: From Pharmacology to Clinical Application.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Role of the long non-coding RNAs in regulation of Gemcitabine response in tumor cells.Cancer cell international · 2023Review
- Abrogation of MAP4K4 protein function causes congenital anomalies in humans and zebrafish.Science advances · 2023Article
- Editorial: Diabetic kidney disease: routes to drug development, pharmacology and underlying molecular mechanisms.Frontiers in pharmacology · 2023Article
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- The Interaction of Apelin and FGFR1 Ameliorated the Kidney Fibrosis through Suppression of TGFOxidative medicine and cellular longevity · 2023Article
- Editorial: Current understanding of complications associated with diabetes.Frontiers in clinical diabetes and healthcare · 2023Article
- Editorial: Receptor biology and cell signaling in diabetes: volume II.Frontiers in pharmacology · 2023Article
- Aberrations inInternational journal of molecular sciences · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
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Authors and funding
9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Endothelial-to-mesenchymal transition (EndMT) has been shown to contribute to organ fibrogenesis, and we have reported that the anti-EndMT effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is associated with restoring expression of diabetes-suppressed fibroblast growth factor receptor (FGFR), the key anti-EndMT molecule. FGFR1 is the key inhibitor of EndMT via the suppression of the transforming growth factor β (TGFβ) signaling pathway, and mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) inhibits integrin β1, a key factor in activating TGFβ signaling and EndMT. Here, we showed that the close proximity between AcSDKP and FGFR1 was essential for the suppression of TGFβ/smad signaling and EndMT associated with MAP4K4 phosphorylation (P-MAP4K4) in endothelial cells. In cultured human dermal microvascular endothelial cells (HMVECs), the anti-EndMT and anti-TGFβ/smad effects of AcSDKP were lost following treatment with a neutralizing FGFR1 antibody (N-FGFR1) or transfection of FRS2 siRNA. The physical interaction between FGFR1 and P-MAP4K4 in HMVECs was confirmed by proximity ligation analysis and an immunoprecipitation assay. AcSDKP induced P-MAP4K4 in HMVECs, which was significantly inhibited by treatment with either N-FGFR1 or FRS2 siRNA. Furthermore, MAP4K4 knockdown using specific siRNAs induced smad3 phosphorylation and EndMT in HMVECs, which was not suppressed by AcSDKP. Streptozotocin-induced diabetic CD-1 mice exhibited suppression of both FGFR1 and P-MAP4K4 expression levels associated with the induction of TGFβ/smad3 signaling and EndMT in their hearts and kidneys; those were restored by AcSDKP treatment. These data demonstrate that the AcSDKP-FGFR1-MAP4K4 axis has an important role in combating EndMT-associated fibrotic disorders.
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