Radiat Oncol. 2026 Jul 16. doi: 10.1186/s13014-026-02892-z. Online ahead of print.
ABSTRACT
Radiation-induced endothelial dysfunction is a critical mechanism underlying long-term cardiovascular and multiorgan toxicity in cancer survivors after radiotherapy. This review integrates current evidence on the molecular pathogenesis, from initial endothelial apoptosis and senescence to the establishment of chronic pro-thrombotic and pro-inflammatory phenotypes involving various signalling pathways. Clinical data reveal that even low to moderate radiation doses can cause sustained endothelial injury, contributing not only to vascular diseases but also to common cerebrovascular and gastrointestinal complications. Advances in vascular imaging and circulating biomarkers facilitate earlier detection of subclinical damage. Promising protective strategies include statins, angiotensin-converting enzyme inhibitors, and pathway-targeted agents. Future research directions include the development of advanced preclinical models and the conduct of large-scale, prospective clinical studies to validate biomarkers and therapeutic interventions, ultimately aiming to integrate vascular preservation into personalized radiotherapy strategies.
PMID:42464324 | DOI:10.1186/s13014-026-02892-z