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Background/Aims: Current knowledge confers a crucial role to connective tissue growth factor (CTGF/CCN2) in hepatic fibrogenesis. Hepatocytes are likely to be the major cellular source of CTGF in the liver in which CTGF is sensitively upregulated by TGF-β. Recently, we demonstrated that the methylxanthine derivate caffeine leads to an upregulation of peroxisome proliferator activated receptor γ (PPARγ) expression in hepatocytes, thus sensitizing these cells to the well-known inhibitory effect of 15-deoxy-Δ12,14-prostaglandin J2 (15-d-PGJ2) on CTGF expression. However, upregulation of the receptor alone is not sufficient per se; its physiological ligand 15-d-PGJ2 is required to exert an inhibitory effect on transforming growth factor-β (TGF-β) target genes such as CTGF. Methods: This study compared serum concentrations of 15-d-PGJ2 in Caucasian patients with fibrotic liver diseases ( n=289), Caucasian controls ( n=136) and Caucasian non-liver disease (NLD) sick ( n=307), as well as of Chinese patients with hepatocellular carcinoma (HCC) ( n=43) and Chinese healthy controls ( n=63) in order to characterize their suitability for therapeutic approaches with PPARγ-inducing (i.e. CTGF inhibitory) drugs such as caffeine. Results: The presented data showed that Caucasian patients with ongoing hepatic fibrogenesis (mean 6.2±5.9 μg/L) displayed strikingly higher serum concentrations of 15-d-PGJ2 than healthy probands (mean 2.3±1.0) and Caucasian patients with NLD (mean 2.7±1.4 μg/L). Similar results were found in Chinese patients with fully developed HCC (mean 1.3±0.7 μg/L) compared with Chinese healthy controls (mean 0.4±0.2 μg/L). Conclusions: In conclusion, our data thus proposed an increased suitability of these patient groups for therapeutic approaches with drugs inducing PPARγ expression, such as methylxanthine derivates. [ABSTRACT FROM AUTHOR]