Abstract
Liver fibrosis leading to cirrhosis and cancer affects millions of people and causes thousands of deaths all over the world. Many signaling pathways could be targeted to block fibrosis but these are not successful. Reviewing recent literature and from our own studies we identified novel target, such as YB-1, which is implicated in inflammation, angiogenesis and accumulation of extracellular matrix (ECM). In addition we observed and showed that the end product of fibrosis, collagen gene, itself is a direct target for controlling fibrosis. We developed triplex-forming oligonucleotides which specifically form triplexes with the promoter of type I procollagen gene and effectively inhibited collagen accumulation and improved liver function. In this review we briefly described the potential of YB-1 and Collagen genes as excellent targets.
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