Key result
Protecting microvascular endothelial cells from radiation-induced perturbations, such as cell death and inflammation, is emerging as a targeted strategy to reduce acute normal tissue radiation damage.
Protecting microvascular endothelial cells from radiation-induced perturbations represents a promising preclinical strategy to mitigate acute normal tissue radiation toxicity.
Endothelial protection may reduce acute radiation toxicity; hypothesis-generating and requires clinical validation before practice change.
Most cancer patients are treated with radiotherapy, but the treatment can also damage the surrounding normal tissue. Radiotherapy side-effects diminish patients' quality of life, yet effective biological interventions for normal tissue damage are lacking. Protecting microvascular endothelial cells from the effects of irradiation is emerging as a targeted damage-reduction strategy. We illustrate the concept of the microvasculature as a mediator of overall normal tissue radiation toxicity through cell death, vascular inflammation (hemodynamic and molecular changes) and a change in functional capacity. Endothelial cell targeted therapies that protect against such endothelial cell perturbations and the development of acute normal tissue damage are mostly under preclinical development. Since acute radiation toxicity is a common clinical problem in cutaneous, gastrointestinal and mucosal tissues, we also focus on damage in these tissues.
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Korpela et al. (2014) conducted a review in Normal tissue radiation damage. Endothelial cell targeted therapies was evaluated. Protecting microvascular endothelial cells from radiation-induced perturbations, such as cell death and inflammation, is emerging as a targeted strategy to reduce acute normal tissue radiation damage.
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