After ischaemia-reperfusion treatment, the Atg7-deficient mice showed aggravated MI/R injury with cardiac hypertrophy, contractile dysfunction, myofibrillar disarray and severe cardiac fibrosis, and CLP36 was found to be accumulated in ischaemia-reperfusion treated Atg7-deficient cardiomyocytes. This evidence concerns the gene ATG7 and cardiac hypertrophy.