ArticleRenal failure2024
LCZ696, an angiotensin receptor-neprilysin inhibitor, ameliorates epithelial-mesenchymal transition of peritoneal mesothelial cells and M2 macrophage polarization.
Article in Renal failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Bibliometric analysis of sacubitril/valsartan in the management of chronic kidney disease (2013-2025).Renal failure · 2026Review
- Host-Pathogen Crosstalk in Pediatric Peritoneal Dialysis-Associated Peritonitis: Molecular Mechanisms Driving Peritoneal Membrane Remodeling.International journal of molecular sciences · 2026Review
- LCZ696 improves oxidative stress injury in human podocytes induced by increased glucose levels via Nrf2/HO-1 signaling pathway.European journal of medical research · 2025Article
- Macrophage-derived cathepsin L promotes epithelial-mesenchymal transition and M2 polarization in gastric cancer.World journal of gastroenterology · 2024Article
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Authors and funding
11 authors.
Funding
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Abstract
aimsTo investigate the effects and mechanisms of LCZ696, an angiotensin receptor-neprilysin inhibitor (ARNI), on epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells and on macrophage M2 polarization.
methodsWe examined the effects of LCZ696 in a 4.25% high glucose peritoneal dialysis fluid (PDF)-induced peritoneal fibrosis (PF) mouse model, and explored the mechanisms of LCZ696 on human peritoneal mesothelial cells (HPMCs) stimulated by TGF-β1 (5 ng/mL) and on Raw264.7 cells stimulated by IL-4 (10 ng/mL). To further elucidate the mechanism, we treated HPMCs with the conditioned medium of Raw264.7 cells.
resultsLCZ696 effectively improved PF and inhibited the process of EMT in PDF mice.
conclusionOur study demonstrated that LCZ696 improves PF and ameliorates TGF-β1-induced EMT of HPMCs by blocking TGF-β/Smad3, PDGFRβ and EGFR pathways. Meanwhile, LCZ696 also inhibits M2 macrophage polarization by regulating STAT6 pathway.
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