Key result
MHC-II-expressing cardiac fibroblasts promote doxorubicin-induced cardiotoxicity and progression to heart failure.
Its licence doesn't allow us to show a copy here.
Why the study?
Doxorubicin cardiotoxicity and progression to heart failure are common adverse effects of anthracycline chemotherapy, with unclear immunological mechanisms involved.
Immunologically active cardiac fibroblasts expressing MHC-II may play a key role in promoting doxorubicin-induced cardiotoxicity.
A common adverse effect of the chemotherapeutic anthracycline, doxorubicin, is cardiotoxicity and progression to heart failure. Patients treated with anthracyclines show increased circulating cytotoxic CD8
No takes yet. Share an insight, caveat, or question.
Zambrano et al. (2026) studied this question. Immunologically active cardiac fibroblasts expressing major histocompatibility complex-II promote doxorubicin-induced cardiotoxicity.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: