Population
Cardiac fibroblasts
Design
Preclinical
Authors
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Suggests Pyk2-Rac1 as antifibrotic target; hypothesis-generating in animal fibroblasts and leaves open human translation.
Angiotensin II activates JNK and c-Jun in cardiac fibroblasts through a Pyk2-dependent, Rac1-mediated pathway independent of EGF-R.
Murasawa et al. (2000) studied this question.
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