Summary
Development of anti-microRNA therapeutic for nonalcoholic fatty liver disease
Nonalcoholic fatty liver disease (NAFLD) initiates with excessive accumulation of liver triglycerides and progresses to nonalcoholic steatohepatitis (NASH), cirrhosis and liver cancer while also modifying brain metabolism. However, NAFLD pathogenesis, the corresponding impact on the brain and the links between them, are poorly understood. In addition NAFLD is largely untreatable. We have discovered that excess microRNA (miR)-132 initiates NAFLD and that miR-132 suppression by oligonucleotide antisense treatment effectively reverses NAFLD in acquired and inherited mouse models. Here we to develop this discovery as a novel and effective pharmaceutical for the treatment of NAFLD, a serious and widespread disease for which there is at present no pharmacological treatment.
Nonalcoholic fatty liver disease (NAFLD) initiates with excessive accumulation of liver triglycerides and progresses to nonalcoholic steatohepatitis (NASH), cirrhosis and liver cancer while also modifying brain metabolism. However, NAFLD pathogenesis, the corresponding impact on the brain and the links between them, are poorly understood. In addition NAFLD is largely untreatable. We have discovered that excess microRNA (miR)-132 initiates NAFLD and that miR-132 suppression by oligonucleotide antisense treatment effectively reverses NAFLD in acquired and inherited mouse models. Here we to develop this discovery as a novel and effective pharmaceutical for the treatment of NAFLD, a serious and widespread disease for which there is at present no pharmacological treatment.
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More information & hyperlinks
| Web resources: | https://cordis.europa.eu/project/id/737590 |
| Start date: | 01-06-2017 |
| End date: | 30-11-2018 |
| Total budget - Public funding: | 150 000,00 Euro - 150 000,00 Euro |
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Original description
Development of anti-microRNA therapeutic for nonalcoholic fatty liver diseaseNonalcoholic fatty liver disease (NAFLD) initiates with excessive accumulation of liver triglycerides and progresses to nonalcoholic steatohepatitis (NASH), cirrhosis and liver cancer while also modifying brain metabolism. However, NAFLD pathogenesis, the corresponding impact on the brain and the links between them, are poorly understood. In addition NAFLD is largely untreatable. We have discovered that excess microRNA (miR)-132 initiates NAFLD and that miR-132 suppression by oligonucleotide antisense treatment effectively reverses NAFLD in acquired and inherited mouse models. Here we to develop this discovery as a novel and effective pharmaceutical for the treatment of NAFLD, a serious and widespread disease for which there is at present no pharmacological treatment.
Status
CLOSEDCall topic
ERC-PoC-2016Update Date
27-04-2024
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