STING promotes CD8 T-cell cardiotropism and fibrosis from distinct cellular compartments in doxorubicin cardiomyopathy
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ID: 316100
2026
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Abstract
AIMS: Doxorubicin (DR), a widely prescribed chemotherapy, has an unfortunate side effect of cardiotoxicity resulting from DNA damage and cardiac cell death. Cardiac atrophy, fibrosis and a cytotoxic CD8+ T-cell response, alongside increased cardiac and circulating interferon-inducible chemokines are hallmarks for DR cardiotoxicity. METHODS AND RESULTS: We discovered that the activation of the Stimulator of Interferon Genes (STING) in several distinct cardiac cell compartments is central to CD8+ T-cell cardiotropism and DR cardiotoxicity. DR activates STING in cardiac fibroblasts (CFB), endothelial cells (EC) and myeloid cells in vivo and in vitro. Myeloid STING is required for CD8+ T-cell activation and cardiotropism, whereas EC STING mediates CD8+ T-cell cardiotropism towards CXCL9/10 and transendothelial migration. In contrast, cardiac fibroblast STING is dispensable for the cardiac CD8+ T-cell immune response but drives fibroblast transformation. We report CXCR3+ T-cells and CXCL9/CXCL10 are more abundant in the hearts of DR cardiotoxicity patients. CONCLUSIONS: Our work positions STING as a cell-specific driver of CD8+ T-cell cardiac inflammation and fibroblast activation in DR cardiotoxicity.
| Reference Key |
openalex_W7163761678
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| Authors | Abraham Bayer, Maria A. Zambrano, Ramona Emig, E Sanders, Sasha Smolgovsky, Noah Wagner, Kenneth C Bedi, Shreyas Bhave, Navin K Kapur, Kenneth B Margulies, A Asnani, Pilar Alcaide |
| Journal | cardiovascular research |
| Year | 2026 |
| DOI |
10.1093/cvr/cvag098
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| URL | |
| Keywords | Keywords not found |
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