Examining potential therapies targeting myocardial fibrosis through the inhibition of transforming growth factor-beta 1.

After injury, the heart undergoes a remodeling process consisting primarily of myocyte hypertrophy, apoptosis and interstitial fibrosis. Although initially beneficial, excess fibrosis gradually results in alteration of left ventricular properties and cardiac dysfunction. Transforming growth factor-beta 1 (TGF-beta(1)) is thought to be a primary mediator of fibrosis within the heart after injury. Currently, angiotensin II blockade is used to inhibit the actions of TGF-beta(1). However, recent studies indicate that angiotensin II blockade alone may not be sufficient to prevent TGF-beta(1)-induced fibrosis. Thus far, both in vivo and in vitro models have shown that direct TGF-beta(1) inhibition, NAPDH oxidase inhibitors, growth factors and hormonal treatment regimens targeting TGF-beta(1) may significantly reduce cardiac fibrosis after injury. This study attempts to underline these alternatives to angiotensin II blockade in combating TGF-beta(1)-induced cardiac dysfunction.