Small RNA profiling in mouse alcohol-induced liver injury and steatosis model.

Complement is known to play a role in alcoholic fatty liver disease (AFLD), but the underlying mechanisms are poorly understood, thereby constraining the development of a rational approach for therapeutic intervention in the complement system.here we demonstrate protection in wild type mice by treatment with CR2-Crry, a C3 inhibitor that specifically targets sites of complement activation. We found that the expression of glycine transfer (t) RNA-derived fragments (Gly-tRFs) is upregulated in ethanol-fed mice, and that inhibition of Gly-tRFs in vivo decreases chronic ethanol-feeding-induced hepatosteatosis without affecting inflammation small RNAs expression profiling of liver tissues obtained after 16 days EtOH feed.