Document Type : Review Article
Authors
1
Department of Clinical Pharmacy, Faculty of Pharmacy, Misr International University, Cairo, Egypt
2
Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University.
3
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Misr International University, Cairo, Egypt.
4
Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt
Abstract
Paclitaxel is a well-known chemotherapeutic agent used to treat various cancers, including breast, lung, and pancreatic cancers. However, its effectiveness is limited by significant adverse effects, including neurotoxicity, nephrotoxicity, hepatotoxicity, testicular toxicity, and cardiotoxicity. In this review, we focused on its potential cardiotoxicity. The mechanisms underlying Paclitaxel-induced cardiotoxicity have not been thoroughly elucidated. In the current review, we highlighted the possible mechanisms involved in Paclitaxel-induced cardiotoxicity. This may include activation of oxidative stress as evident by elevation in cellular lipid peroxidation, and decrease in Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx), and Catalase (CAT) activity. Moreover, oxidative stress induces cell death, as well as activation of the inflammatory response. Paclitaxel-induced inflammation was evident by the release of inflammatory cytokines and chemokines. In addition, ferroptosis, which is a form of cell death characterized by accumulation of iron, is thought to be a possible underlying mechanism of Paclitaxel-induced cardiotoxicity. Furthermore, Paclitaxel causes cardiotoxicity through stimulation of apoptotic pathways. Taking all together, Paclitaxel-induced cardiotoxicity affects the quality of life of cancer patients and is considered a challenge facing pharmaceutical research nowadays.
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