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<p>The present study investigates how Sirtuin 1 (SIRT1) regulates the worsening of calcium oxalate (CaOx) crystal-induced mitochondrial dysfunction and fibrosis in the kidneys with age. To establish a CaOx crystal deposition model, glyoxylic acid (Gly) was injected intraperitoneally into both young and aged mice. Additionally, an in vitro model was created by stimulating human renal tubular epithelial (HK2) cells with D-galactose (D-gal) and calcium oxalate monohydrate (COM). Lipid deposition, mitochondrial function, and fibrosis levels were assessed using various techniques, including western blotting (WB), polymerase chain reaction (PCR), immunohistochemistry, immunofluorescence, and specific staining methods. The effects on lipid deposition, mitochondrial function, and fibrosis were further analyzed by manipulating the expression of SIRT1 and peroxisome proliferator-activated receptor (PPAR-α), both in vitro and in vivo. Aging exacerbates the kidney mitochondrial dysfunction and fibrosis induced by CaOx crystals, with SIRT1 playing a crucial regulatory role in this process. SIRT1 regulates lipid metabolism via PPARα, intensifying the aging-related kidney mitochondrial damage and fibrosis induced by CaOx crystals.</p>

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SIRT1 regulates CaOx crystal-induced exacerbation of renal mitochondrial dysfunction and fibrosis through PPAR-α in aged mice

  • 期刊论文

  • 发表日期：

    2026年5月29日

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  • Yuexian Xu,
  • Kaiguo Xia,
  • Xike Mao,
  • Junfeng Yao,
  • Bingbing Hou,
  • Wei Wang,
  • Zongyao Hao

摘要

The present study investigates how Sirtuin 1 (SIRT1) regulates the worsening of calcium oxalate (CaOx) crystal-induced mitochondrial dysfunction and fibrosis in the kidneys with age. To establish a CaOx crystal deposition model, glyoxylic acid (Gly) was injected intraperitoneally into both young and aged mice. Additionally, an in vitro model was created by stimulating human renal tubular epithelial (HK2) cells with D-galactose (D-gal) and calcium oxalate monohydrate (COM). Lipid deposition, mitochondrial function, and fibrosis levels were assessed using various techniques, including western blotting (WB), polymerase chain reaction (PCR), immunohistochemistry, immunofluorescence, and specific staining methods. The effects on lipid deposition, mitochondrial function, and fibrosis were further analyzed by manipulating the expression of SIRT1 and peroxisome proliferator-activated receptor (PPAR-α), both in vitro and in vivo. Aging exacerbates the kidney mitochondrial dysfunction and fibrosis induced by CaOx crystals, with SIRT1 playing a crucial regulatory role in this process. SIRT1 regulates lipid metabolism via PPARα, intensifying the aging-related kidney mitochondrial damage and fibrosis induced by CaOx crystals.