The mechanisms responsible for the increased hepatic connective tissue deposition in cirrhosis remain unknown; and there is no established therapy for hepatic fibrosis. In this issue of Hepatology, Ruwart et al. (1) report that 16,16-dimethyl prostaglandin E2 (DMPG) inhibits hepatic collagen deposition, and, therefore, potentially will be effective in the treatment of cirrhosis. This editorial will first review the assembly of extracellular matrix (ECM) proteins and the metabolism of collagens, the most abundant proteins in the ECM. Using this knowledge of connective tissue proteins as a framework, strategies for the therapy of hepatic fibrosis will be discussed.
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Chojkier et al. (1988) studied this question.
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