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

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.

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Publication Details

Journal
Scientific Reports
Published
2025-11-19
DOI
https://doi.org/10.1038/s41598-025-25204-z
Citations
2
Primary Topic
Ferroptosis and cancer prognosis
Type
article
Field-Weighted Citation Impact
3.04
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Bone marrow mesenchymal stem cells-derived exosomes protect against β-cell destruction models and kidney injury by suppressing ferroptosis

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Scientific Reports
Ferroptosis and cancer prognosis
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article

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

Dongwei Liu, Zhihong Liu, Sijie Zhou, Linbo Wang, Zhangsuo Liu, Jiahui Zhang
article en
2 citations

Abstract

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.

Scientific ReportsVol. 15(1)
Nanjing General Hospital of Nanjing Military Command (CN), Zhengzhou University (CN), First Affiliated Hospital of Zhengzhou University (CN), Nanjing University (CN)
Openalex Percentile: Top 7%
Ferroptosis and cancer prognosis
3.04
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