Conditional PAI-1 deletion in the endothelial compartment has no beneficial effect on radiation-induced whole-lung damage in mice

Radiation pneumonitis and radiation-induced lung fibrosis are common side effects of thoracic tumor treatment. Mechanisms of radiation-induced lung damage include breakdown of the alveolar-capillary barrier and endothelial activation. Plasminogen activator inhibitor type 1 (PAI-1) has been identified as an interesting therapeutic target against lung fibrosis by knockout of the PAI-1 gene or pharmaceutical inhibition of PAI-1. Our aim was to investigate whether the endothelial pool of PAI-1 plays a role in the development of radiation-induced lung damage, as previously demonstrated in the intestine.

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