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<p>Lipid disorder is an independent risk factor of diabetic kidney disease (DKD). Excess accumulation of lipid in podocytes can cause cell dysfunction and cell death. Chaperone-mediated autophagy (CMA) serves as a critical role in regulating lipid metabolism. However, the exact role of CMA in the podocytes of DKD with dyslipidemia is still uncertain. Herein, we aimed to explore the role of CMA in hyperlipidemia-induced lipid accumulation and apoptosis in podocytes. In the present study, we showed that palmitic acid (PA) treatment induced the activation of CMA, increased lipid accumulation and apoptosis in podocytes. We further found that blocking CMA with inhibitor VER155008 or LAMP-2&#xa0;A siRNA significantly upregulated PA-induced increased expression of PLIN2, exacerbated PA-induced lipid accumulation and apoptosis, whereas promoting CMA with Torin1 downregulated the expression of PLIN2, ameliorated lipid accumulation and apoptosis in PA-induced podocytes. Moreover, we also observed the activation of CMA and increased lipid accumulation in the kidney tissue of DKD mice. Taken together, these results suggest that CMA plays a protective role in PA-induced podocytes apoptosis and that the potential protective mechanism of CMA is involved in reducing cellular lipid accumulation through mediating the degradation of PLIN2.</p>

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Chaperone-mediated autophagy ameliorates hyperlipidemia-induced apoptosis in podocytes via attenuating lipid accumulation

  • 期刊论文

  • 发表日期：

    2026年1月7日

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  • Wenge Huang,
  • Lingke Xu,
  • Xuemei Chen,
  • Xushun Jiang,
  • Xiaogang Du

摘要

Lipid disorder is an independent risk factor of diabetic kidney disease (DKD). Excess accumulation of lipid in podocytes can cause cell dysfunction and cell death. Chaperone-mediated autophagy (CMA) serves as a critical role in regulating lipid metabolism. However, the exact role of CMA in the podocytes of DKD with dyslipidemia is still uncertain. Herein, we aimed to explore the role of CMA in hyperlipidemia-induced lipid accumulation and apoptosis in podocytes. In the present study, we showed that palmitic acid (PA) treatment induced the activation of CMA, increased lipid accumulation and apoptosis in podocytes. We further found that blocking CMA with inhibitor VER155008 or LAMP-2 A siRNA significantly upregulated PA-induced increased expression of PLIN2, exacerbated PA-induced lipid accumulation and apoptosis, whereas promoting CMA with Torin1 downregulated the expression of PLIN2, ameliorated lipid accumulation and apoptosis in PA-induced podocytes. Moreover, we also observed the activation of CMA and increased lipid accumulation in the kidney tissue of DKD mice. Taken together, these results suggest that CMA plays a protective role in PA-induced podocytes apoptosis and that the potential protective mechanism of CMA is involved in reducing cellular lipid accumulation through mediating the degradation of PLIN2.