AGONISTS OF DDAH1 FOR TREATING ENDOTHELIAL DYSFUNCTION

摘要

The present invention derives from the finding that expression of DDAH1 is heavily post- transcriptionally regulated by microRNAs. By preventing or blocking the interaction between such microRNAs and the DDAH1 mRNA, the production of DDAH1 protein can be increased. This has utility in the prevention or treatment of diseases and disorders that are associated with reduced DDAH1 levels or increased ADMA levels, such as diseases or disorders that are characterised by endothelial dysfunction.