Key result
CDK 4/6 inhibitors may cause cardiovascular toxicity in breast cancer despite limited mechanistic data.
Why the study?
Breast cancer treatment cardiotoxicity significantly affects survivors' quality of life, but few studies address the cardiovascular toxicity of CDK 4/6 inhibitors.
What are the cardiovascular toxicities and related mechanisms caused by CDK 4/6 inhibitors in patients with advanced breast cancer?
What are the cardiovascular toxicities and related mechanisms caused by CDK 4/6 inhibitors in patients with advanced breast cancer?
This review summarizes the potential cardiovascular toxicities and underlying mechanisms associated with CDK 4/6 inhibitors used in the treatment of advanced breast cancer.
Answers are grounded in this paper and cite their sources.
May warrant CV monitoring with CDK4/6 inhibitors; leaves open incidence, mechanisms, and mitigation strategies.
Breast cancer is the most common malignant tumour in women, and it has a high incidence and mortality rate both in the world and in China. Hormone receptor-positive breast cancer accounts for about 60–70% of breast cancer and is the most common subtype of advanced breast cancer. Cyclin-dependent kinase 4 and 6 (CDK 4/6) inhibitors in combination with endocrine therapy have emerged as the treatment of choice for hormone receptor-positive and human epidermal growth factor receptor 2-negative advanced breast cancer. Emergence inhibitors of CDK 4/6 have significantly improved outcomes in patients with hormone receptor-positive advanced breast cancer. It is an indisputable fact that cardiotoxicity caused by breast cancer treatment can have a significant impact on the quality of life of cancer survivors; however, there are few studies on the cardiovascular toxicity of CDK 4/6 inhibitors. This article reviews the cardiovascular toxicity and related mechanisms that may be caused by CDK 4/6 inhibitors.
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Zhang et al. (2025) studied this question. CDK 4/6 inhibitors for hormone receptor-positive breast cancer may cause cardiovascular toxicity, but evidence and mechanism data remain limited.
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