ArticleClinical and experimental nephrology2022
Role of IGF-1R in epithelial-mesenchymal transdifferentiation of human peritoneal mesothelial cells.
Article in Clinical and experimental nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- A review of research progress on mechanisms of peritoneal fibrosis related to peritoneal dialysis.Frontiers in physiology · 2023Review
- Immune micro-environment and drug analysis of peritoneal endometriosis based on epithelial-mesenchymal transition classification.Frontiers in endocrinology · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPeritoneal fibrosis (PF) is caused by epithelial-mesenchymal transdifferentiation (EMT) in the peritoneum under high glucose (HG) conditions. The study aimed to explored the role of Insulin-like growth factor 1 receptor (IGF-1R) in the regulation of EMT in human peritoneal mesothelial cells (HPMCs).
methodsWe used HG peritoneal dialysis fluid (PDF) to induce in vivo PF in mice, and treated HPMCs with HG in vitro to stimulate EMT.
resultsIn the mice, the higher the glucose concentration in the dialysate, the more obvious the peritoneal tissue thickening and the more that collagen was deposited. The in vitro study indicated that the expression of IGF-1R, α-SMA, vimentin was upregulated, while the expression of occludin, ZO-1, and E-cadherin was downregulated in HPMCs under HG and IGF-1R overexpression conditions. Conversely, the expression of IGF-1R, α-SMA, and vimentin was downregulated, while the expression of occludin, ZO-1, and E-cadherin was upregulated in IGF-1R-underexpressed HPMCs under HG conditions. The cell migration abilities were increased, while the cell adhesion abilities were reduced in HPMCs under HG and IGF-1R overexpression conditions. In contrast, cell migration abilities were reduced, while cell adhesion abilities were increased in IGF-1Runderexpressed HPMCs under HG conditions.
conclusionsTargeting at IGF-1R may provide novel insights into the prevention and treatment of PF.
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Registered trials
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