This editorial highlights the first direct human evidence that chronic NF-kappa B activation links radiation exposure to sustained vascular inflammation, offering a potential molecular target to prevent radiation-induced cardiovascular disease.
Radiation injury of blood vessels was originally described more than a century ago and remains a contemporary clinical problem, despite dramatic advances in the field of radiation oncology (1). Clinical studies indicate that patients who have previously undergone radiation therapy for various malignancies—such as lymphoma, breast cancer, and head and neck cancer—are at increased risk for developing vascular disease (2). The consequences are significant; depending upon the study, the relative risk of suffering a clinical cardiovascular event (i.e., myocardial infarction, stroke) related to radiation therapy ranges from approximately 1.5- to 4.0-fold, and this risk is further amplified in the presence of traditional cardiovascular risk factors (3,4).
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Weintraub et al. (2010) conducted an editorial in Radiation-induced vascular disease in cancer survivors. Radiation therapy exposure vs. Nonirradiated arteries was evaluated on NF-kappa B up-regulation and pro-inflammatory gene expression in human arteries.
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