Cardiac Remodelling Following Cancer Therapy: A Review
Tan Panpan1, Du Yuchen2, Shi Xianyong3
1Puyang Medical College, Henan, 457000, China. pyyz_tpp@126.com.
Insights
Cancer therapies like chemotherapy and immunotherapy can cause cardiac remodelling, leading to heart damage. This review explains the mechanisms behind these heart changes induced by anti-cancer treatments.
Area of Science:
- Cardiology
- Oncology
- Pharmacology
Background:
- Cardiac remodelling involves detrimental changes in heart structure and function.
- These changes include alterations in size, shape, fibrosis, and inflammation, potentially leading to heart failure.
Purpose of the Study:
- To elucidate the fundamental mechanisms of cardiac remodelling induced by various cancer therapies.
- To provide a comprehensive overview of how anti-cancer treatments affect heart health.
Main Methods:
- This is a review article, synthesizing existing research on cancer therapy-induced cardiotoxicity.
- The review examines mechanisms of cardiac damage from radiation and specific drug classes.
Main Results:
- Radiation and anti-cancer drugs (chemotherapy, RTKIs, ICIs) can induce cardiac remodelling.
- Mechanisms include inflammation, fibrosis, and vascular remodelling, impacting heart function.
Conclusions:
- Understanding these mechanisms is crucial for managing cardiotoxicity in cancer patients.
- Further research can inform strategies to mitigate heart damage during cancer treatment.
Abstract:
Cardiac remodelling is characterized by abnormal changes in the function and morphological properties such as diameter, mass, normal diameter of cavities, heart shape, fibrosis, thickening of vessels and heart layers, cardiomyopathy, infiltration of inflammatory cells, and some others. These damages are associated with damage to systolic and diastolic abnormalities, damage to ventricular function, and vascular remodelling, which may lead to heart failure and death. Exposure of the heart to radiation or anti-cancer drugs including chemotherapy drugs such as doxorubicin, receptor tyrosine kinase inhibitors (RTKIs) such as imatinib, and immune checkpoint inhibitors (ICIs) can induce several abnormal changes in the heart structure and function through the induction of inflammation and fibrosis, vascular remodelling, hypertrophy, and some others. This review aims to explain the basic mechanisms behind cardiac remodelling following cancer therapy by different anti-cancer modalities.
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