Rac2 plays an important role in bleomycin-induced lung injury, according to researchers who say it is an important signaling molecule leading to BLM-induced mortality. It also mediates the physiological changes seen in the airways after BLM-induced injury.

Pulmonary fibrotic diseases induce significant morbidity and mortality, for which there are limited therapeutic options available. Rac2, a ras-related guanosine triphosphatase expressed mainly in hematopoietic cells, is a crucial molecule regulating a diversity of mast cell, macrophage, and neutrophil functions, researchers said.

All these cell types have been implicated in the development of pulmonary fibrosis in a variety of animal models. For their study, researchers hypothesized that Rac2 deficiency protects mice from bleomycin-induced pulmonary fibrosis.