ArticleScientific reports2025
Cyanidin-3-glucoside upregulated NDRG2 through the PI3K/AKT pathway to alleviate EMT and ECM in renal fibrosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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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, 1 synthesis or guideline pooled it.
- Hepato-Renal Axis: A Systematic Review of Anthocyanin Protective Mechanisms of Preclinical Evidence.Molecular nutrition & food research · 2026Pooled it
- Mechanistic Insights into Aldose Reductase-Dependent Modulation of Hypoxia-Inducible Factor-1α in Promoting Renal Fibrosis.Cell biochemistry and biophysics · 2026Article
- Research Progress and Prospects of Flavonoids in the Treatment of Diseases by Regulating Autophagy: A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Renal fibrosis is a critical progression of chronic kidney disease, and epithelial-to-mesenchymal transition (EMT) and extracellular matrix(ECM) deposition are crucial pathologic change of renal fibrosis, which still lacks of effective treatment. In this study, it was found that cyanidin-3-O-glucoside (C3G) could inhibit EMT and ECM activated by unilateral ureteral obstruction (UUO) and transforming growth factor-β1 (TGF-β1) stimulation. Moreover, N-Myc downstream-regulated gene 2(NDRG2), which involved in the progression of renal fibrosis, was down-regulated in vivo and in vitro model. However, C3G pretreatment could reverse the reductive expression of NDRG2. Furthermore, we found that the combined treatment of C3G and si-NDRG2 could reverse the decreased EMT and ECM, which induced by C3G treatment only. And the activation of Phosphatidylinositol 3-kinase (PI3K)/ Protein Kinase B (AKT) pathway significantly enhanced EMT and ECM, which was decreased by C3G treatment only in TGF-β1 induced Human Kidney 2 (HK-2) cells. In conclusion, our results demonstrated that C3G alleviated EMT and ECM by elevating NDRG2 expression through the PI3K/AKT pathway, indicating that C3G could be a potential treatment against renal fibrosis.
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