Despite technological advancements in RT techniques, which enhance tumor targeting precision and minimize incidental cardiac doses, late cardiac toxicity remains a concern. Various pathological processes, such as cardiomyopathy, conduction disorders, myocardial fibrosis, pericarditis, acute coronary syndrome, congestive heart failure, and valvular disease, contribute to radiation-induced heart disease (RIHD) development.
These processes involve complex interactions between cellular types, altered wound healing, and activation of proinflammatory signaling pathways. Collagen deposition and fibrosis development are well-characterized consequences of heart exposure to RT, leading to conditions like pericarditis, cardiomyopathy, arrhythmias, congestive heart failure, or sudden death. Radiation-induced myocardial fibrosis (RIMF) is a significant outcome of RIHD, particularly common in RT-treated thoracic cancer patients. RIMF is a progressive, largely irreversible process resulting from complex multicellular interactions. Despite ongoing research, the mechanisms behind radiation-induced myocardial fibrosis (RIMF) remain poorly understood, and effective clinical treatments are still lacking, significantly affecting the quality of life for long-term cancer survivors. We are actively researching novel strategies aimed at mitigating or reversing the progression of RIMF.