In the pathophysiology of PE, FN1 is involved in several molecular mechanisms that contribute to the development and progression of the disease, such as vascular remodeling and angiogenesis, inflammation and modulation of the immune response, oxidative stress, endothelial dysfunction, dysregulation of growth factors, and the restructuring of the extracellular matrix; furthermore, the clinical pathophysiology of PE may be related to dysfunctional FN1 plasma levels [15]. Here, FN1 is linked to endothelial dysfunction.