Myocardial fibrosis in TGF-beta1 transgenic mice is driven by complex MMP and TIMP regulation, highlighting potential therapeutic targets for myocardial diseases.
May identify antifibrotic targets in myocardial disease; leaves open human translation pending further studies.
TGF-beta(1) produces myocardial fibrosis in vivo. This effect is not only produced by a stimulation of matrix protein formation: a complex regulation of MMP and TIMP interaction, namely decrease of expression and activity of interstitial collagenase and an enhanced inhibition by increased levels of TIMPs, are involved. These mechanisms are optional targets for therapeutic interventions in myocardial diseases.
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Seeland et al. (2002) studied this question.
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