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<p>Bone marrow mesenchymal stem cell-derived exosomes (BMSC-EXOs) exhibit therapeutic potential in type 1 diabetes mellitus (T1D). In a streptozotocin (STZ)-induced T1D mouse model, BMSC-EXOs reduced hyperglycemia, prevented weight loss, and alleviated early-stage diabetic kidney injury. These protective effects were associated with preserving pancreatic islet structure, restoring β-cell insulin production, and reducing oxidative stress. Mechanistically, BMSC-EXOs inhibited ferroptosis by up-regulating Glutathione peroxidase 4 (GPX4) expression, decreasing lipid peroxidation, and preventing β-cell and kidney damage. These findings indicate that BMSC-EXOs protect against STZ-induced β-cell destruction models and T1D-related complications by inhibiting ferroptosis, presenting a potential therapeutic approach for diabetes management.</p>

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Bone marrow mesenchymal stem cells-derived exosomes protect against β-cell destruction models and kidney injury by suppressing ferroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月19日

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  • Jiahui Zhang,
  • Linbo Wang,
  • Dongwei Liu,
  • Zhangsuo Liu,
  • Zhihong Liu,
  • Sijie Zhou

摘要

Bone marrow mesenchymal stem cell-derived exosomes (BMSC-EXOs) exhibit therapeutic potential in type 1 diabetes mellitus (T1D). In a streptozotocin (STZ)-induced T1D mouse model, BMSC-EXOs reduced hyperglycemia, prevented weight loss, and alleviated early-stage diabetic kidney injury. These protective effects were associated with preserving pancreatic islet structure, restoring β-cell insulin production, and reducing oxidative stress. Mechanistically, BMSC-EXOs inhibited ferroptosis by up-regulating Glutathione peroxidase 4 (GPX4) expression, decreasing lipid peroxidation, and preventing β-cell and kidney damage. These findings indicate that BMSC-EXOs protect against STZ-induced β-cell destruction models and T1D-related complications by inhibiting ferroptosis, presenting a potential therapeutic approach for diabetes management.