We have subsequently shown that resistin overexpression induced cardiac hypertrophy with impaired Ca2+ handling, and insulin resistance in isolated cardiomyocytes28 while long-term cardiac-specific overexpression of resistin in vivo significantly decreased left ventricular contractility and induced a complex phenotype of oxidative stress, fibrosis, apoptosis and myocardial remodeling in normal rats, producing a phenotype resembling diabetic cardiomyopathy29,37. Here, RETN is linked to cardiac hypertrophy.