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. 2015 Apr 17;93(9):1045–1055. doi: 10.1007/s00109-015-1282-2

Fig. 6.

Fig. 6

Summary diagram: hepatic overexpression of miR-26a in mice alleviates ethanol-induced hepatic steatosis and liver injury by augmenting autophagic degradation of lipid droplets. Overexpression of miR-26a increases the expression of the autophagy mediator Beclin-1, which is regulated by mitogen-activated protein kinases. DUSP4 and DUSP5, two MAPK inhibitors, were identified as direct targets of miR-26a. Several other negative regulators of autophagy, such as MCL1, TAB2, COX5A, and POLR3G, were also identified as potential targets of miR-26a. Forced expression of miR-26a in the liver can alleviate ethanol-induced hepatic steatosis and liver injury by augmenting the autophagic degradation of lipid droplets in hepatocytes