Nevertheless, targeting osteopontin with a specific aptamer was beneficial in treating LV remodeling and dysfunction in wild-type TAC mice [126], suggesting that complete loss of osteopontin might lead to more severe cardiac dysfunction due to either attenuated or exaggerated myocardial fibrosis, whereas partial osteopontin blocking with pharmacological agents (aptamers) seems to be beneficial. This evidence concerns the gene SPP1 and Myocardial fibrosis.