STING promotes CD8 T-cell cardiotropism and fibrosis from distinct cellular compartments in doxorubicin cardiomyopathy - PubMed
5 hours ago
- #STING pathway
- #Doxorubicin cardiotoxicity
- #CD8 T-cells
- STING activation in distinct cardiac cell compartments drives CD8 T-cell cardiotropism and fibrosis in doxorubicin-induced cardiomyopathy.
- Myeloid STING is necessary for CD8 T-cell activation and cardiotropism, while endothelial STING facilitates T-cell migration via CXCL9/10.
- Cardiac fibroblast STING promotes fibroblast transformation independent of the T-cell immune response.
- Increased CXCR3+ T-cells and CXCL9/CXCL10 are observed in hearts of patients with doxorubicin cardiotoxicity.
- STING is identified as a cell-specific regulator of cardiac inflammation and fibrosis in doxorubicin cardiotoxicity.