Changing the Pathogenetic Roadmap of Liver Fibrosis? Where Did It Start; Where Will It Go?

Olav A. Gressner; Mohamed S. Rizk; Evgeniya Kovalenko; Ralf Weiskirchen; Axel M. Gressner


J Gastroenterol Hepatol. 2008;23(7):1024-1035. 

In This Article


Despite intensive experimental studies, the clinical opportunities for patients with fibrosing liver diseases have not yet significantly improved. It is expected that increasing knowledge of new pathogenetic mechanisms, which complement the 'canonical principle' of fibrogenesis, will have a beneficial effect on the translation to clinical medicine. It is now evident that the heterogeneous pool of (myo-)fibroblasts originates from the EMT of cholangiocytes and most likely of hepatocytes, from the influx of bone marrow-derived fibrocytes into the damaged liver tissue and from differentiation of a subgroup of circulating monocytes to fibroblasts after homing in the damaged tissue. These processes offer innovative diagnostic and therapeutic options. As an example, modulation of the TGF-ß/BMP-7 ratio changes the rate of EMT and by this progression of fibrosis. Over-expression of BMP-7[172] or application of recombined BMP-7[148,157,158] have a sustained antifibrotic effect. In addition, the determination of some of these parameters and of connective tissue growth factor (CTGF)[173] in serum might provide information on fibrogenic activity. Thus, the pathogenetic road map of fibrosis has not (yet?) changed, but newly discovered backstreets now establish a much more complex network of interacting pathways radiating to systemic responses.

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