Abstract
To the Editor: Kuwahara et al1 report a very interesting study in which transforming growth factor (TGF)-β is demonstrated to have a pivotal role in myocardial fibrosis and diastolic dysfunction. They elegantly show that repeated administration of an anti-TGF-β neutralizing antibody inhibits fibroblast activation, collagen induction, and myocardial fibrosis, and also reverses diastolic dysfunction in pressure-overloaded rats. They conclude that TGF-β blockade may be a “potential” therapeutic strategy. Investigations involving ocular wound healing models have shown a similar pattern of TGF-β activity to that described by Kuwahara et al1 in their cardiac model, with peak TGF-β expression occurring predominantly in fibroblasts at …
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