Abstract: The present invention contemplates that lysophosphatidic acid (LPA) may be induced by lung injury and may be responsible for aberrant wound-healing responses. For example, in a bleomycin model of pulmonary fibrosis LPAi deficient mice are protected from pulmonary fibrosis and mortality. Specifically, chemotactic-induced fibroblast responses, lung fibroblast accumulation, and vascular permeability increases were all attenuated. In contrast, however, bleomycin-induced leukocyte recruitment was preserved. These results demonstrate that LPAi activity may link pulmonary fibrosis with lung injury by mediating fibroblast recruitment and vascular leak. The present invention therefore represents LPAi as a new target to treat lung diseases including, but not limited to, fibrosis, idiopathic pulmonary fibrosis, and acute respiratory distress syndrome.