Therapies that specifically retard progression or induce regression of fibrotic liver disease have entered the clinical stage [1,2]. This is remarkable, since clinical validation of antifibrotic efficacy remains difficult and since the mere reduction of excess scarring, without an improvement of hepatic angio-architecture and synthetic function is a disputed primary clinical endpoint [3]. Importantly, as in cancer therapies, drugs that address more than a single pathogenic pathway are usually more efficient than single highly specific pathway modulators [1].
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Zhang et al. (2014) studied this question.
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