Furthermore, genetic deletion of low-density lipoprotein receptor (LDLr) by using adeno-associated virus vector serotype 8 (AAV8) has been found to counteract pressure-overload-induced cardiac hypertrophy, cardiomyocyte apoptosis, diastolic dysfunction, and interstitial and perivascular myocardial fibrosis in TAC-treated female LDLr−/− mice [33]. This evidence concerns the gene LDLR and Myocardial fibrosis.