Vitamin D3 attenuates doxorubicin-induced senescence of human aortic endothelial cells by upregulation of IL-10 via the pAMPKα/Sirt1/Foxo3a signaling pathway.
basic_science · Level V
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- Record sourced from PubMed, PMID 34101754.
- Also identified by DOI 10.1371/journal.pone.0252816 and PMC identifier 8186764.
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Abstract
The toxicity of doxorubicin to the cardiovascular system often limits its benefits and widespread use as chemotherapy. The mechanisms involved in doxorubicin-induced cardiovascular damage and possible protective interventions are not well-explored. Using human aortic endothelial cells, we show vitamin D3 strongly attenuates doxorubicin-induced senescence and cell cycle arrest. We further show the protective effects of vitamin D3 are mediated by the upregulation of IL-10 and FOXO3a expression through fine modulation of pAMPKα/SIRT1/FOXO3a complex activity. These results have great significance in finding a target for mitigating doxorubicin-induced cardiovascular toxicity.
Medical subject headings
- Cellular Senescence
- Cholecalciferol
- Doxorubicin
- Endothelial Cells
- Interleukin-10
- Proteins
- Signal Transduction