Myofibrillogenesis regulator1 (MR1) was first identified from a human skeletal muscle cDNA library in the laboratory, and the previous studies have proved the role of MR1 in Angiotensin Ⅱ(AngⅡ) -induced cardiac hypertrophy both in vivo and in vitro. However, relevant underlying molecular mechanisms of MR1 in AngⅡ induced cardiac hypertrophy remain to be elucidated. Gene silencing of MR1 by adenovirus-delivered siRNA approach in mice was used, and microarray analysis of myocardial gene expressions was compared before and after MR1 silencing along with AngⅡ treatment. Significant changes of genes expression in several pathways, such as pathways involved in cardiac hypertrophy and mTOR signaling etc., were observed between the two groups. Furthermore, genes that were changed by 10 folds after MR1 silencing were totally listed, with 39 genes being down-regulated and 5 up-regulated. To further verify the microarray results, some of genes that are suggested to be closely related to cardiac hypertrophy were detected by quantitative RT-PCR. As a result, HSP72 and thioredoxin 1 (Trx1) expression were increased, while the calcineurin Phosphatase β(CnAβ) and β-myosin (β-myosin) expression were suppressed upon MR1 silencing. These signaling pathways and genes are closely correlated with cardiac hypertrophy induced by Ang Ⅱ. The alterations of relevant pathways and genes may help understand the molecular role of MR1 in AngⅡ-induced cardiac hypertrophy.