Chemotherapy agents cause severe cardiovascular complications, with approximately 10% of cancer patients succumbing to cardiovascular problems, highlighting the need for novel multi-OMICs therapies.
Multi-OMICs approaches offer a promising avenue for identifying novel biomarkers and therapeutic targets to mitigate chemotherapy-induced cardiotoxicity.
Chemotherapy-induced cardiotoxicity is a critical issue in cardio-oncology, as cancer treatments often lead to severe cardiovascular complications. Approximately 10% of cancer patients succumb to cardiovascular problems, with lung cancer patients frequently experiencing arrhythmias, cardiac failure, tamponade, and cardiac metastasis. The cardiotoxic effects of anti-cancer treatments manifest at both cellular and tissue levels, causing deformation of cardiomyocytes, leading to contractility issues and fibrosis. Repeated irradiation and chemotherapy increase the risk of valvular, pericardial, or myocardial diseases. Multi-OMICs analyses reveal that targeting specific pathways as well as specific protein modifications, such as ubiquitination and phosphorylation, could offer potential therapeutic alternatives to current treatments, including Angiotensin converting enzymes (ACE) inhibitors and beta-blockers that mitigate symptoms but do not prevent cardiomyocyte death, highlighting the need for more effective therapies to manage cardiovascular defects in cancer survivors. This review explores the xenobiotic nature of chemotherapy agents and their impact on cardiovascular health, aiming to identify novel biomarkers and therapeutic targets to mitigate cardiotoxicity.
Ma et al. (Wed,) conducted a review in Chemotherapy-induced cardiotoxicity. Chemotherapy agents was evaluated. Chemotherapy agents cause severe cardiovascular complications, with approximately 10% of cancer patients succumbing to cardiovascular problems, highlighting the need for novel multi-OMICs therapies.