ArticleMolecular medicine reports2019
Zinc supplementation inhibits the high glucose‑induced EMT of peritoneal mesothelial cells by activating the Nrf2 antioxidant pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 13 citations in OpenAlex.
- Adjuvant therapy with zinc supplementation; anti-inflammatory and anti-oxidative role in multiple myeloma patients receiving autologous hematopoietic stem cell transplantation: a randomized controlled clinical trial.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Trial
- Zinc Supplementation Sustains Diaphragm Contractility and PreservesBiomolecules · 2026Article
- NRF2 and Thioredoxin Reductase 1 as Modulators of Interactions between Zinc and Selenium.Antioxidants (Basel, Switzerland) · 2024Article
- The activation of HAMP promotes colorectal cancer cell proliferation through zinc-mediated upregulation of SMAD4 expression.Translational cancer research · 2024Article
- Zinc: a potential star for regulating peritoneal fibrosis.Frontiers in pharmacology · 2024Review
- Progress in the study of nutritional status and selenium in dialysis patients.Annals of medicine · 2023Review
- Zinc Deficiency Exacerbates Bisphenol A-Induced Hepatic and Renal Damage: Delineation of Molecular Mechanisms.Biological trace element research · 2023Article
- The antioxidative effects of empagliflozin on high glucose‑induced epithelial-mesenchymal transition in peritoneal mesothelial cells via the Nrf2/HO-1 signaling.Renal failure · 2022Article
- Mechanisms of Peritoneal Mesothelial Cells in Peritoneal Adhesion.Biomolecules · 2022Review
- Diet in Intestinal Fibrosis: A Double-Edged Sword.Nutrients · 2021Review
- Asiaticoside inhibits TGF-β1-induced mesothelial-mesenchymal transition and oxidative stress via the Nrf2/HO-1 signaling pathway in the human peritoneal mesothelial cell line HMrSV5.Cellular & molecular biology letters · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high glucose (HG)‑induced epithelial‑mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) serves an important role in peritoneal fibrosis (PF) during peritoneal dialysis. Our previous study reported that zinc (Zn) supplementation prevented the HG‑induced EMT of rat PMCs in vitro. In the present study, the role of Zn in HG‑induced EMT was investigated in vivo using a rat model of PF. Additionally, the molecular mechanisms underlying HG‑induced EMT were studied in human PMCs (HPMCs). In the rat model of PF, HG treatment increased the glucose transfer capacity and decreased the ultrafiltration volume. Histopathological analysis revealed peritoneal thickening, increased expression of vimentin and decreased expression of E‑cadherin. ZnSO4 significantly ameliorated the aforementioned changes, whereas Zn inhibition by clioquinol significantly aggravated the effects of HG on rats. The effects of Zn on HPMCs was assessed using western blot analysis, Transwell assays and flow cytometry. It was revealed that Zn also significantly suppressed the extent of the EMT, and reduced reactive oxygen species production and the migratory ability of HG‑induced HPMCs, whereas Zn inhibition by N',N',N',N'‑tetrakis (2‑pyridylmethyl) ethylenediamine significantly potentiated the HG‑induced EMT of HPMCs. HG‑stimulated HPMCs exhibited increased expression of nuclear factor‑like 2 (Nrf2) in the nucleus, and total cellular NAD(P)H quinone dehydrogenase 1 (NQO1) and heme oxygenase-1 (HO‑1), the target proteins of the Nrf2 antioxidant pathway. Zn supplementation further promoted nuclear Nrf2 expression, and increased the expression of target proteins of the Nrf2 antioxidant pathway, whereas Zn depletion decreased nuclear Nrf2, NQO1 and HO‑1 expression compared with the HG group. In conclusion, Zn supplementation was proposed to suppress the effects of HG on the EMT by stimulating the Nrf2 antioxidant pathway and subsequently reducing oxidative stress in PMCs.
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