ArticleScientific reports2026
LncRNA MALAT1 drives diabetic kidney injury via Nrf2 suppression in glomerular endothelium.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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12 authors.
Funding
Abstract
To investigate the role of LncRNA MALAT1 in insulin resistance (IR) and and oxidative stress injury in hunman glomerular endothelial cells (HGECs) under high glucose and insulin (HG/Ins) conditions, and to elucidate its regulatory mechanism involving the Nrf2 pathway. HGECs were exposed to 25 mM glucose and 100 nM insulin for 48 h to induce insulin resistance. MALAT1 was silenced by siRNA, with knockdown efficiency verified via qPCR. Given the critical role of Nrf2 in oxidative stress regulation, Nrf2 inhibitor ML385 and activator SFN were used to explore the pathway-dependent mechanism. Accordingly, experimental groups included control, ML385, and SFN. Groups included control, ML385, and SFN. Protein expression, Reactive Oxygen Species (ROS), apoptosis, and Nrf2 translocation were assessed by Western blot, flow cytometry, and immunofluorescence. Following IR induction in HGECs (25 mM glucose + 100 nM insulin, 48 h) and siRNA-mediated MALAT1 knockdown, effects on proteins, ROS, apoptosis, and Nrf2 translocation were assessed in control and modulator groups. MALAT1 exacerbates IR and oxidative stress-induced injury in HGECs by inhibiting Nrf2 nuclear translocation. Targeting the MALAT1-Nrf2 axis may serve as a novel strategy for diabetic kidney disease (DKD).
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