ArticleExperimental and therapeutic medicine2018
Silence of IGFBP7 suppresses apoptosis and epithelial mesenchymal transformation of high glucose induced-podocytes.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Renal insulin-like growth factor binding-protein 7 is a critical promoter of progressive diabetic kidney disease.Nature communications · 2025Article
- 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
- Article
- The Circ_35953 induced by the NF-κB mediated the septic AKI via targeting miR-7219-5p/HOOK3 and IGFBP7 axis.Journal of cellular and molecular medicine · 2023Article
- Senescence of Tumor Cells in Anticancer Therapy-Beneficial and Detrimental Effects.International journal of molecular sciences · 2022Review
- ATF4-dependent heme-oxygenase-1 attenuates diabetic nephropathy by inducing autophagy and inhibiting apoptosis in podocyte.Renal failure · 2021Article
- Increased IGFBP7 Expression Correlates with Poor Prognosis and Immune Infiltration in Gastric Cancer.Journal of Cancer · 2021Article
- The aqueous extract of Lycopus lucidus Turcz exerts protective effects on podocytes injury of diabetic nephropathy via inhibiting TGF-β1 signal pathway.American journal of translational research · 2019Article
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
Insulin-like growth factor-binding protein 7 (IGFBP7) has been identified as a secreted protein associated with a number of cellular processes. However, the specific regulatory mechanisms of IGFBP7 on podocytes of diabetic nephropathy (DN) are yet to be elucidated. In the present study, podocytes were identified initially via an immunofluorescence assay using an anti-synaptopodin antibody. It was subsequently demonstrated that glucose promoted podocyte proliferation in a time- and dose-dependent manner via MTT assay. In addition, IGFBP7 expression was silenced in podocytes via siRNA, the effects of which were evaluated using western blotting and reverse transcription-quantitative polymerase chain reaction. It was demonstrated that silencing IGFBP7 inhibited apoptosis and epithelial mesenchymal transformation (EMT) of podocytes mediated by high glucose (HG). Transforming growth factor (TGF)-β1/mothers against decapentaplegic homolog (Smad) signaling was associated with proliferation, apoptotic activities and EMT. Therefore, the expression levels of TGF-β1/Smad pathway were detected, and it was observed that silencing IGFBP7 suppressed the TGF-β1/Smad pathway in podocytes induced by HG. These findings suggested that IGFBP7 may serve as a potential therapeutic target for DN.
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Registered trials
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.