The heart responds to diverse forms of stress by hypertrophic growth accompanied 
by fibrosis and eventual diminution of contractility, which results from 
down-regulation of alpha-myosin heavy chain (alphaMHC) and up-regulation of 
betaMHC, the primary contractile proteins of the heart. We found that a 
cardiac-specific microRNA (miR-208) encoded by an intron of the alphaMHC gene is 
required for cardiomyocyte hypertrophy, fibrosis, and expression of betaMHC in 
response to stress and hypothyroidism. Thus, the alphaMHC gene, in addition to 
encoding a major cardiac contractile protein, regulates cardiac growth and gene 
expression in response to stress and hormonal signaling through miR-208.