Key result
Cyclophosphamide induces dose-dependent cardiotoxicity, with an incidence of 8-20% in adults and 5% in children at doses over 120-150 mg/kg.
Why the study?
Cyclophosphamide causes dose-dependent cardiotoxicity that limits its clinical use, and understanding its molecular mechanisms and signaling pathways is needed to help develop new therapies.
What are the molecular mechanisms and incidence of cyclophosphamide-induced cardiotoxicity?
What are the molecular mechanisms and incidence of cyclophosphamide-induced cardiotoxicity?
Cyclophosphamide causes dose-dependent cardiotoxicity, and understanding its molecular mechanisms may help develop new cardioprotective therapies.
Monitor for cardiotoxicity with high-dose cyclophosphamide; review leaves open optimal prevention strategies.
One of the commonest antitumor drugs is cyclophosphamide (CP). CP that is used in management of many tumors and autoimmune disease as well as in polychemotherapy regimens and immunosuppressive protocols. It doesn't only have a specific effect on cancer cells, but also it produces many toxic effects. One of the most important side effects of CP that limits its use in clinical practice is its dose dependent toxicity on the heart. The incidence of cardiotoxicity at doses over 120-150 mg/kg is of 8-20% in adults, and 5% in children. The incidence of heart failure after high doses of CP varies widely from author to author: less than 5% and 10-29%.This review article discusses the molecular mechanism of CP cardiotoxicity with some of different signaling pathways that contribute in the development of such toxicity. Our main concern from discussing these molecular mechanisms of CP induced cardiotoxicity is to help in development of new therapies.
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Kamel et al. (2022) conducted a review in Cyclophosphamide-induced cardiotoxicity. Cyclophosphamide was evaluated on Cardiotoxicity and heart failure. Cyclophosphamide induces dose-dependent cardiotoxicity, with an incidence of 8-20% in adults and 5% in children at doses over 120-150 mg/kg.
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