ArticleImmunity, inflammation and disease2023
Bone marrow stromal cell-derived exosomes improve oxidative stress and pyroptosis in doxorubicin-induced myocardial injury in vitro by regulating the transcription of GSDMD through the PI3K-AKT-Foxo1 pathway.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes Preserve Melanocyte Stem Cell Integrity Under Acute Neurogenic Oxidative Stress via Activation of the Nrf2-ARE Pathway in C57BL/6J Mice.Journal of cosmetic dermatology · 2026Article
- LncRNA MEG3 inhibits glioma progression by inducing pyroptosis through the miR-223-3p/FOXO1/PARP1 axis.American journal of cancer research · 2026Article
- Extracellular Vesicles in the Heart-Organ Axis: From Inter-Organ Communication to Precision Nanomedicine for Heart Diseases.International journal of nanomedicine · 2026Review
- Exosome‑mediated crosstalk between the cardiovascular and musculoskeletal systems: Mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Pyroptosis: candidate key targets for mesenchymal stem cell-derived exosomes for the treatment of bone-related diseases.Stem cell research & therapy · 2025Review
- Research progress on pyroptosis regulated by mesenchymal stem cell-derived exosomes.Frontiers in immunology · 2025Review
- Potential Signal Pathways and Therapeutic Effects of Mesenchymal Stem Cell on Oxidative Stress in Diseases.Current pharmaceutical design · 2025Review
- [MiR-224-5p overexpression inhibits oxidative stress by regulating the PI3K/Akt/FoxO1 axis to attenuate hypoxia/reoxygenation-induced cardiomyocyte injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Exosomal miR-9-5p derived from iPSC-MSCs ameliorates doxorubicin-induced cardiomyopathy by inhibiting cardiomyocyte senescence.Journal of nanobiotechnology · 2024Article
- Bone marrow stromal cell-derived exosomes improve oxidative stress and pyroptosis in doxorubicin-induced myocardial injury in vitro by regulating the transcription of GSDMD through the PI3K-AKT-Foxo1 pathway.Immunity, inflammation and disease · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesDoxorubicin (DOX) can contribute to severe myocardial injury, and bone marrow stromal cells (BMSC)-exosomes (Exos) improves acute myocardial infarction. Hence, this research investigated whether BMSC-Exos alleviated DOX-induced myocardial injury.
methodsBMSC-derived Exos were isolated and identified, and the optimal concentration of DOX was confirmed. H9C2 cells were treated with DOX and BMSC-Exos or in combination with the protein kinase B (AKT) inhibitor. Reactive oxygen species (ROS) and JC-1 were detected to assess oxidative stress (OS) and mitochondrial membrane damage, respectively. In addition, the expression of pyroptosis-related molecules was measured. The expression of phosphatidylinositol 3 kinase (PI3K)-AKT pathway-related proteins and the phosphorylation and acetylation of forkhead box O1 (Foxo1) in the cell nucleus and cytoplasm were tested. Last, interactions between Foxo1 and gasdermin D (GSDMD) were assessed.
resultsBMSC-Exo treatment increased viability and mitochondrial membrane potential and reduced lactic dehydrogenase release and ROS levels in DOX-treated H9C2 cells. Furthermore, the addition of BMSC-Exos suppressed DOX-induced activation and upregulation of NLRP3 and apoptosis-associated speck-like protein containing A CARD (ASC) and in vitro cleavage of caspase-1, GSDMD, interleukin (IL)-1β, and IL-18 proteins. Additionally, BMSC-Exo treatment enhanced the expression of phosphorylated (p)-PI3K, p-AKT, and p-mTOR in DOX-treated H9C2 cells and the levels of phosphorylated Foxo1 in the cytoplasm of DOX-treated H9C2 cells. Foxo1 was enriched in the promoter region of GSDMD. Moreover, the AKT inhibitor API-2 annulled the effects of BMSC-Exos on OS, pyroptosis, and Foxo1 phosphorylation in DOX-treated H9C2 cells.
conclusionsBMSC-Exos phosphorylated Foxo1 and inactivated Foxo1 transcription via the PI3K-AKT pathway to diminish GSDMD expression, thus restraining DOX-induced pyroptosis and OS of myocardial cells.
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