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Possibility of DIF-1, a small molecule which regulates the transdifferentiation of HSC, as a therapeutic agent for liver fibrosis

Fibrosis occurs in major organs, such as the heart, kidney, liver, and pancreas. The fibrotic organs eventually become dysfunctional. Fibrosis is also observed in cancer development and involved in the formation of tumor microenvironment. Fibrosis has so far been considered as an irreversible condition, having focused on the prevention rather than the treatment. However, several recent reports have shown that fibrotic state is reversible and proposed new therapeutic strategies for fibrosis treatment. Fibrosis is caused by excessive accumulation of extracellular matrix (ECM). Although ECM-secreting cells are different in different organs where fibrosis is organ-specifically induced, some mechanisms for fibrosis are likely common in these organs. Thus, understanding fibrosis in a cross-organ manner may be great benefit for the development of new therapeutic approaches. In this symposium, we present and discuss the latest results of our fibrosis research targeting ECM-producing cells in various organs, which allow us to deepen our understanding of fibrosis mechanism and to develop new approaches for fibrosis therapy.<br />

Advanced approaches to fibrosis treatment by considering various organs

The 142nd Annual Meeting of the Pharmaceutical Society of Japan (Nagoya)

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[GS02-5]Possibility of DIF-1, a small molecule which regulates the transdifferentiation of HSC, as a therapeutic agent for liver fibrosis

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