ArticleEuropean journal of medical research2026
METTL14 knockdown mitigates HG-induced HK-2 cell apoptosis, inflammation, and ferroptosis by promoting SLC40A1.
Article in European journal of medical research, 2026. 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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Who cites it
2 citing papers in PubMed.
- Transcriptomic and genetic evidence highlights EHHADH in a FUNDC1-associated mitochondrial network in diabetic nephropathy.Metabolism open · 2026Article
- IRF9-dependent transcriptional regulation of SLC40A1 suppresses ferroptosis in dilated cardiomyopathy.Scientific reports · 2026Article
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4 authors.
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Abstract
backgroundDiabetic nephropathy (DN) represents a leading cause of chronic kidney diseases worldwide. While solute carrier family 40 member 1 (SLC40A1) is involved in the regulation of iron homeostasis and iron transport in diabetic kidney disease, its specific role and underlying mechanism in regulating ferroptosis during DN progression remain elusive.
methodsProtein and mRNA expression levels were detected using western blot and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. Cell viability and apoptosis were measured using the cell counting kit-8 (CCK8) and flow cytometry assays. The tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), ferrous iron (Fe
resultsSLC40A1 levels were decreased in high glucose (HG)-induced HK-2 cells. Notably, SLC40A1 overexpression abolished HG-induced action of cell viability, cell apoptosis, inflammation, and ferroptosis. Mechanistically, silencing SLC40A1 greatly reversed the protective roles of METTL14 knockdown in HG-induced damage and ferroptosis of HK-2 cells. In addition, in vivo, SLC40A1 mitigated kidney damage, inflammation, and ferroptosis.
conclusionsMETTL14 knockdown remits HG-induced HK-2 cell apoptosis, inflammation, and ferroptosis via promoting SLC40A1. In addition, E2F4 enhances SLC40A1 transcription. This research provides new potential targets and insights for the treatment of DN.
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