During radiotherapy, vascular remodeling plays a critical role in the response of tissues to radiation. The process involves dynamic changes in the phenotype and function of blood vessels within the irradiated area. Initially, radiation exposure leads to endothelial cell damage and disruption of vascular integrity, triggering inflammatory responses. This results in the release of cytokines, growth factors, and chemokines, which promote endothelial cell proliferation and migration. In addition, pericytes, a more recently identified cellular actor in radiation response, are recruited to damaged vessels. Ultimately, this remodeling process aims to restore tissue perfusion and oxygenation, and facilitates intra-tumoral drug distribution. However, it can also contribute to tumor progression, treatment resistance and normal tissue toxicity if dysregulated. Understanding the intricate mechanisms of vascular remodeling during radiotherapy is crucial for optimizing treatment outcomes and minimizing side effects.
Ultra-high dose rate (UHDR/Flash) radiotherapy is an emerging radiation therapy technique that delivers a high dose of radiation in a fraction of a second. UHDR radiotherapy has been shown to minimize damage to surrounding healthy tissues while effectively targeting cancer cells (Flash effect). This Flash effect is dependent on tissue oxygenation, yet a clear explanation of its radioprotective mechanisms remains elusive. Our group is currently focusing on comprehensively understanding the vascular effects of Flash radiotherapy and their implications in both normal and tumor tissue radiosensitivity.