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<p>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&#xa0;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&#xa0;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).</p>

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LncRNA MALAT1 drives diabetic kidney injury via Nrf2 suppression in glomerular endothelium

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月9日

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  • Li-rong Yang,
  • Hui Wang,
  • Li-rui Jia,
  • Li-ting Cao,
  • Hong-yan Luo,
  • Jia-mei Ding,
  • Yan-song Wang,
  • Yun-peng Tang,
  • Ya-bo Chen,
  • Xiao He,
  • Xin-Tao,
  • Ya-li Zheng

摘要

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).