COL3A1 and myocardial infarction: Col3a1 was of particular interest, because it was down-regulated in response to exercise in mice (1.6, 3.1-fold) and rats (1.8-fold) but up-regulated in most pathological cardiac hypertrophy models, including αMHC403/+ mice (2.2-fold), aortic binding in mice (3.1-fold) and rats (1.6-fold), arteriovenous shunt (1.7-fold), myocardial infarction (2.5-fold), and idiopathic and ischemic cardiac hypertrophy in humans (1.5- and 2.0-fold, respectively).