Key result
Cyclophosphamide-induced cardiotoxicity is a significant concern in hematopoietic stem cell transplantation, and targeting the anti-angiogenic effects of its metabolite acrolein represents a promising therapeutic approach.
Why the study?
Cyclophosphamide-induced cardiotoxicity remains an unresolved issue, particularly in post-HSCT settings, and the exact underlying mechanisms are not fully elucidated.
This review highlights the mechanisms and potential therapeutic targets, such as acrolein's anti-angiogenic effect, for managing cyclophosphamide-induced cardiotoxicity in post-HSCT patients.
Answers are grounded in this paper and cite their sources.
Cardiotoxicity risk persists with low-dose cyclophosphamide post-HSCT; leaves open exact mechanisms and targeted prevention.
Cyclophosphamide-induced cardiotoxicity, associated with its toxic metabolite acrolein, is a significant concern and unresolved issue, especially when cyclophosphamide is administrated in high doses. However, cardiotoxicity following low-dose cyclophosphamide has been also documented, especially in post-hematopoietic stem cell transplantation (post-HSCT) settings. Despite the involvement of multiple signaling pathways in cyclophosphamide-induced cardiomyopathy, the exact underlying mechanisms remain to be fully elucidated. This review outlines the current challenges of cyclophosphamide therapy in HSCT recipients. In addition, the promising therapeutic approaches by targeting acrolein's anti-angiogenic effect were thoroughly discussed to better manage post-HSCT cyclophosphamide-induced cardiotoxicity.
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Alizadehasl et al. (2024) conducted a review in Cyclophosphamide-induced cardiotoxicity. Cyclophosphamide was evaluated. Cyclophosphamide-induced cardiotoxicity is a significant concern in hematopoietic stem cell transplantation, and targeting the anti-angiogenic effects of its metabolite acrolein represents a promising therapeutic approach.
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