Cancer Drugs Spark Cardiac Concerns

New Research Uncovers Mechanisms of Heart Damage

As cancer survival rates climb, a growing number of patients face the unintended consequence of heart damage from life-saving treatments. Emerging research highlights specific drugs and therapies contributing to cardiotoxicity, prompting a call for heightened vigilance.

Ribociclib’s Impact on Heart Tissue

The CDK4/6 inhibitor ribociclib, used in certain cancer therapies, has demonstrated cardiotoxic effects, particularly heart failure. Research presented at the European Society of Cardiology (ESC) Cardio-Oncology Annual Conference suggests this damage may stem from impaired spliceosome assembly, a crucial cellular process.

“Overexpression of E2F1 in these cardiomyocytes was performed, resulting in a threefold increase in expression of the E2F1 protein, which mitigated these ribociclib-induced cardiac effects.”

—Eva Pet, PhD Candidate

Preclinical studies using engineered heart tissues revealed that ribociclib treatment led to significant cardiac dysfunction, including tissue dilation and reduced contractile force. Researchers found that boosting the E2F1 protein’s expression helped to counteract these harmful effects, indicating a potential pathway to mitigate damage.

“Overexpression of E2F1 in these cardiomyocytes was performed, resulting in a threefold increase in expression of the E2F1 protein, which mitigated these ribociclib-induced cardiac effects.” –EVA PET, PhD CANDIDATE pic.twitter.com/a4k4v9eD2g

— ASCO Post (@ascopost) August 15, 2025

GBP5: A Potential Shield Against Radiation Damage

Thoracic radiation therapy, while effective against cancer, can also lead to cardiac fibrosis. New research is focusing on guanylate-binding protein 5 (GBP5), a protein implicated in the inflammatory response following radiation.

A study involving mice with a modified GBP5 molecule, which lacks a key component for inflammasome assembly, showed remarkable protection against radiation-induced cardiac damage and mortality. This suggests that targeting GBP5 could be a promising strategy to preserve heart function after radiation treatment.

“GBP5 is a potential therapeutic target to reduce cardiac damage after radiation.”

– Markus Benjamin Heckmann, MD

Ibrutinib and Atrial Fibrillation: A Mitochondrial Link

The Bruton’s tyrosine kinase (BTK) inhibitor ibrutinib, used for certain blood cancers, is associated with cardiovascular risks, including atrial fibrillation. Investigations are now pointing to mitochondria, the powerhouses of cells, as a key area affected by ibrutinib.

Using advanced imaging techniques on atrial-specific heart cells, researchers observed significant, dose-dependent changes in mitochondrial structure following ibrutinib exposure. These alterations suggest that impaired mitochondrial function may underlie the development of atrial fibrillation linked to this medication.

In the United States, approximately 18.6 million people have a history of cancer, and this number is projected to surpass 22 million by 2035, highlighting the widespread impact of these treatment-related side effects (American Cancer Society).

Future Directions in Cardio-Oncology

The insights gained from these studies are crucial for developing safer and more effective cancer therapies. By understanding the precise mechanisms of cardiotoxicity, clinicians can implement better monitoring strategies and explore novel therapeutic targets to protect patients’ cardiovascular health during cancer treatment.