ArticleRegenerative therapy2022
NUP160 knockdown inhibits the progression of diabetic nephropathy
Article in Regenerative therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Antifibrotic Effects of Yi-Qi-Jian-Pi-Xiao-Yu Formula in Kidney via HIF1A-Driven M1 Macrophage Polarization.Phytochemical analysis : PCA · 2026Article
- STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress.Toxicology research · 2024Article
- ANGPTL4 May Regulate the Crosstalk Between Intervertebral Disc Degeneration and Type 2 Diabetes Mellitus: A Combined Analysis of Bioinformatics and Rat Models.Journal of inflammation research · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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Abstract
Diabetic nephropathy (DN) is a severe diabetic complication and podocyte damage is a hallmark of DN. The Nucleoporin 160 (NUP160) gene was demonstrated to regulate cell proliferation and apoptosis in mouse podocytes. This study explored the possible role and mechanisms of NUP160 in high glucose-triggered podocyte injury. A rat model of DN was established by intraperitoneal injection of 60 mg/kg streptozotocin (STZ). Podocytes were treated with 33 mM high glucose. The effects of the Nup160 on DN and its mechanisms were assessed using MTT, flow cytometry, Western blot, ELISA, RT-qPCR, and luciferase reporter assays. The
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