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<p>Cyclophosphamide (CPA) is an alkylating drug utilized in the treatment of several cancers and autoimmune illnesses. Liver injury is a serious adverse effect linked to the administration of CPA. Nonetheless, the mechanism behind this toxicity remains incompletely elucidated; mechanistic investigations have identified oxidative stress, inflammatory responses, and apoptosis as pivotal elements contributing to CPA-induced liver dysfunction. In addition, CPA triggers the production of reactive oxygen species that act as damage-associated molecular patterns that rapidly activate TLR4/MYD88/NF-κB and NLRP3 inflammasome signaling cascades. Additionally, Nrf2/HO-1, α-klotho, and P-AMPK, which have anti-inflammatory and antioxidative characteristics, are thought to be important signaling pathways that mitigate oxidative stress in CPA-induced liver dysfunction. This review comprehensively covers all aspects of liver injury, including its epidemiology of drug-induced liver injury, risk factors, clinical presentation, chemotherapy-induced liver injury severity index, pathogenesis of CPA-induced liver injury and molecular mechanisms, and therapeutic choices. This study seeks to consolidate all known data about CPA-evoked liver injury, focusing on the probable redox molecular pathways underlying CPA-induced liver injury and recent drugs that showed a protective impact. In conclusion, studying these molecular pathways might open the way for early alleviation of hepatic dysfunction.</p>

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Unraveling chemotherapy-evoked hepatic dysfunction: a deep dive into cyclophosphamide-related liver injury

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年9月27日

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  • Ehab E. Sharata,
  • Mina Ezzat Attya,
  • Marwa M. Khalaf,
  • Remon Roshdy Rofaeil,
  • Ramadan A. M. Hemeida,
  • Amira M. Abo-Youssef

摘要

Cyclophosphamide (CPA) is an alkylating drug utilized in the treatment of several cancers and autoimmune illnesses. Liver injury is a serious adverse effect linked to the administration of CPA. Nonetheless, the mechanism behind this toxicity remains incompletely elucidated; mechanistic investigations have identified oxidative stress, inflammatory responses, and apoptosis as pivotal elements contributing to CPA-induced liver dysfunction. In addition, CPA triggers the production of reactive oxygen species that act as damage-associated molecular patterns that rapidly activate TLR4/MYD88/NF-κB and NLRP3 inflammasome signaling cascades. Additionally, Nrf2/HO-1, α-klotho, and P-AMPK, which have anti-inflammatory and antioxidative characteristics, are thought to be important signaling pathways that mitigate oxidative stress in CPA-induced liver dysfunction. This review comprehensively covers all aspects of liver injury, including its epidemiology of drug-induced liver injury, risk factors, clinical presentation, chemotherapy-induced liver injury severity index, pathogenesis of CPA-induced liver injury and molecular mechanisms, and therapeutic choices. This study seeks to consolidate all known data about CPA-evoked liver injury, focusing on the probable redox molecular pathways underlying CPA-induced liver injury and recent drugs that showed a protective impact. In conclusion, studying these molecular pathways might open the way for early alleviation of hepatic dysfunction.