“…Indeed, several integrin-associated signaling proteins, including integrin-linked kinase (ILK, Zhang et al, 2006; Li et al, 2009; Kavvadas et al, 2010; Shafiei and Rockey, 2012; Radovanac et al, 2013), focal adhesion kinase (FAK, Wong et al, 2011; Lagares et al, 2012; Kinoshita et al, 2013; Lagares and Kapoor, 2013; Zhao et al, 2016), and regulators and effectors of Rho GTPases, such as P-Rex1 (Liang et al, 2016), PAK and Rho-activated kinase (ROCK, Knipe et al, 2015; Martin et al, 2016) have been identified as potential targets for anti-fibrotic therapy in a number of organs. Notably, activation of ILK, which links F-actin to focal adhesions and is required for integrin-mediated force generation, sustains nuclear YAP accumulation in pulmonary arterial vascular smooth muscle cells to promote cell proliferation in pulmonary arterial hypertension, a disease characterized by increased deposition of extracellular matrix and vascular stiffness (Kudryashova et al, 2016).…”