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Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
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Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Jue Li1, Lusha Zhang2, Teng Ge2

  • 1Engineering Research Center of Brain Health Industry of Chinese Medicine, Key Laboratory of Pharmacodynamics and Material Basis of Chinese Medicine of Shaanxi Administration of Traditional Chinese Medicine, Pharmacology of Chinese medicine, Shaanxi University of Chinese Medicine, Xianyang, 712046, People's Republic of China.

Drug Design, Development and Therapy
|March 25, 2024
PubMed

Insights

Sorafenib, a tyrosine kinase inhibitor (TKI), effectively treats cancers like HCC and RCC but causes cardiovascular issues. Understanding these mechanisms, including endothelial dysfunction and ferroptosis, is key to managing side effects and improving cancer therapy.

Area of Science:

  • Oncology
  • Cardiology
  • Pharmacology

Background:

  • Tyrosine kinase inhibitors (TKIs) target vascular endothelial growth factor receptor (VEGFR) for cancer treatment.
  • Sorafenib, a VEGFR and RAF inhibitor, is used for hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC).
  • TKIs, including sorafenib, are associated with significant cardiovascular adverse effects like hypertension and cardiac dysfunction.

Purpose of the Study:

  • To explore the mechanisms behind sorafenib-induced cardiovascular adverse effects.
  • To discuss potential therapeutic strategies for mitigating these side effects.
  • To highlight the link between sorafenib's cardiovascular toxicity, efficacy, and emerging factors like glycolysis.

Main Methods:

  • Literature review of mechanisms underlying sorafenib's cardiovascular toxicity.
  • Analysis of potential treatment strategies including antioxidants and renin-angiotensin system inhibitors.
  • Examination of emerging research on sorafenib-induced glycolysis and drug resistance.

Main Results:

  • Sorafenib-induced cardiovascular toxicity involves endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, autophagy, and ferroptosis.
  • Hypertension is a notable side effect linked to sorafenib's efficacy.
  • Emerging evidence suggests a connection between sorafenib-induced glycolysis, drug resistance, and cardiovascular toxicity.

Conclusions:

  • Understanding the mechanisms of sorafenib's cardiovascular toxicity is crucial for optimizing cancer treatment.
  • Developing targeted strategies can help minimize cardiovascular risks associated with sorafenib therapy.
  • Further research is needed to fully elucidate the role of glycolysis in sorafenib's toxicity and resistance.
Keywords:
cancercardiovascular toxicityhypertensionsorafenibvascular endothelial growth factor receptor

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