ArticleJournal of molecular histology2020
Lefty-1 inhibits renal epithelial-mesenchymal transition by antagonizing the TGF-β/Smad signaling pathway.
Article in Journal of molecular histology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
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- The Expression of miR-377-3p in Patients with DKD and the Regulatory Mechanism of miR-377-3p on the Inflammatory Response of HK-2 Cells Through TGF-β.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- MiR-449a downregulation alleviates the progression of renal interstitial fibrosis by mediating the KLF4/MFN2 axis.International urology and nephrology · 2023Article
- Fibrotic Response of Human Trabecular Meshwork Cells to Transforming Growth Factor-Beta 3 and Autotaxin in Aqueous Humor.Biomolecules · 2022Article
- Small extracellular vesicles encapsulating lefty1 mRNA inhibit hepatic fibrosis.Asian journal of pharmaceutical sciences · 2022Article
- Construction of Endometrial Carcinoma ceRNA Network and Screening of Key Genes Based on TCGA Database.Computational and mathematical methods in medicine · 2022Article
- Lefty1 Ameliorates Post-infarction Fibrosis by Suppressing p-Smad2 and p-ERK1/2 Signaling Pathways.Journal of cardiovascular translational research · 2021Article
- Developments for Collagen Hydrolysate in Biological, Biochemical, and Biomedical Domains: A Comprehensive Review.Materials (Basel, Switzerland) · 2021Review
- Overexpression of ring finger protein 20 inhibits the progression of liver fibrosis via mediation of histone H2B lysine 120 ubiquitination.Human cell · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a biological process in which tubular epithelial cells lose their phenotypes, and new mesenchymal feature are obtained. In particular, type II EMT possibly contributes to renal tissue fibrogenesis. Recent studies indicate that Lefty-1, a novel member of the TGF-β superfamily with pleiotropical and biological regulation characteristics on TGF-β and other signaling pathways, is considered to have potential fibrotic effects. However, its role in EMT, which is often a long-term consequence of renal tubulointerstitial fibrosis, remains unknown. In this study, we found that Lefty-1 alleviates EMT induction through antagonizing TGF-β/Smad pathway in vivo and in vitro. In unilateral ureteral obstruction (UUO) model mice, administration of adenovirus-mediated overexpression of Lefty-1 (Ad-Lefty-1) significantly reduced TGF-β1/Smad expression and alleviated the phenotypic transition of epithelial cells to mesenchymal cells and extracellular matrix (ECM) accumulation. In high glucose-induced rat renal tubular duct epithelial cell line (NRK-52E), EMT and ECM synthesis were alleviated with Lefty-1 treatment, which significantly inhibited TGF-β1/Smad pathway activation in UUO mice and high glucose-treated NRK-52E cells. Thus, Lefty-1 can alleviate EMT and renal interstitial fibrosis in vivo and in vitro through antagonizing the TGF-β/Smad pathway, and Lefty-1 might have a potential novel therapeutic effect on fibrotic kidney diseases.
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