AGT and Myocardial fibrosis: Interestingly, cardiac fibroblasts, isolated from osteopontin-null mice, maintained their ability to produce components of ECM but displayed altered proliferation and adhesion, suggesting that attenuated myocardial fibrosis in osteopontin-null mice in the Ang-II induced model of LV hypertrophy may be related to the cardiac fibroblast properties and not necessarily to the ECM synthesis [59].