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Hepatology. 2009 Sep;50(3):970-8. doi: 10.1002/hep.23097.

Less Smad2 is good for you! A scientific update on coffee's liver benefits.

Author information

1
Institute of Clinical Chemistry and Pathobiochemistry, Central Laboratory, RWTH University Hospital, Aachen, Germany. ogressner@ukaachen.de

Abstract

Scientists at the National Institutes of Health have reported that increased coffee consumption is associated with a slower progression of fibrogenesis in patients with chronic and particularly alcoholic liver disease and a reduced incidence of heptocellular carcinoma. However, a causal mechanistic explanation was pending. New results indicate that the methylxanthine caffeine--a major component of coffee and the most widely consumed pharmacologically active substance in the world--might be responsible for this phenomenon, because it inhibits the synthesis of connective tissue growth factor (CTGF/CCN2) in liver parenchymal and nonparenchymal cells, primarily by inducing degradation of Smad2 (and to a much lesser extent Smad3) and thus impairment of transforming growth factor beta (TGF-beta) signaling. CTGF and TGF-beta play crucial roles in the fibrotic remodeling of various organs, and, ultimately, carcinogenesis. This article summarizes the clinical-epidemiological observations as well as the pathophysiological background and provides suggestions for the therapeutic use of (methyl)xanthine derivatives in the management of fibro-/carcinogenic (liver) diseases.

PMID:
19610047
DOI:
10.1002/hep.23097
[Indexed for MEDLINE]

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