Page 73 - CIBEREHD2016-ENG

Most relevant scientific articles
• Klionsky DJ, Abdelmohsen K, Abe A, Abedin MJ, Abeliovich H, Acevedo Arozena A et al. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy. 2016;12(1):1- 222.
• Morales-Ibanez O., Affo S., Rodrigo-Torres D., Blaya D., Millan C., Coll M. et al. Kinase analysis in alcoholic hepatitis identifies p90RSK as a potential mediator of liver fibrogenesis. Gut. 2016.
• Prieto-Dominguez N., Ordonez R., Fernandez A., Mendez-Blanco C., Baulies A., Garcia-Ruiz C. et al. Melatonin-induced increase in sensitivity of human hepatocellular carcinoma cells to sorafenib is associated with reactive oxygen species production and mitophagy. Journal of Pineal Research. 2016.
• Blaya D., Coll M., Rodrigo-Torres D., Vila-Casadesus M., Altamirano J., Llopis M. et al. Integrative microRNA profiling in alcoholic hepatitis reveals a role for microRNA-182 in liver injury and inflammation. Gut. 2016.
• Nuno-Lambarri N., Dominguez-Perez M., Baulies-Domenech A., Monte M.J., Marin J.J.G., Rosales- Cruz P. et al. Liver Cholesterol Overload Aggravates Obstructive Cholestasis by Inducing Oxidative Stress and Premature Death in Mice. Oxidative Medicine and Cellular Longevity. 2016;2016.
Hightlights
The most relevant activities performed during 2016 centered on the identification of new therapeutic targets in patients with alcoholic steatohepatitis and the characterization of new cytotoxic mechanisms of sorafenib and events associated with its resistance in hepatocellular carcinoma, including the disruption
of mitophagy and the catabolism of the ceramide through glucosilceramide synthase induction. In relation with the processes of autophagy, we have participated in an international initiative to elaborate the guides for the assays and interpretation of autophagy and its implications in physiopathological processes. Furthermore, we have identified that hepatocellular free cholesterol plays a key role in obstructive cholestasis due to the increase of the mitochondrial oxidative stress and alterations in the expression of the antioxidant defenses. During 2016 we have received financial support from the NIH/NIAAA through
an agreement with the University of Southern California (USC Los Angeles, CA) to investigate the role
of mitochondrial cholesterol and StARD1 in alcoholic liver disease. As a result of the above-mentioned action, we have generated a chimeric StARD1 floxed mice that have been crossed with Alb-Cre or Mxl-Cre
to produce mice with selective deficiency of StARD1 in hepatocytes or myeloid cells, respectively and these results are now in consideration. Finally, one of the most prominent aspects during 2016 has been the development of a mouse (FRGN) that allows the repopulation of the mouse liver with human hepatocytes and human hematopoietic cells, which will serve as a great translational research tool for the study of human liver diseases, an activity that has been partly supported from a strategic action from the CIBEREHD.
EHD
research Groups 73