PLAU and apparent mineralocorticoid excess: APE is also associated with inflammatory response and part of the protective action of exogenous uPA might be due to the ability to uPAR to inhibit signaling pathways associated with inflammation and cell death (Zagorski et al., 2003; Zhang et al., 2007; Wang et al., 2009; Apostolakis and Spandidos, 2013; Wang et al., 2013; Wang et al., 2014; Zhang et al., 2017; Shi et al., 2018), in turn alleviating APE-associated ischemia and pulmonary hypertension.