Liver fibrogenesis remains a significant outcome of chronic liver disease and etiologic factors of progression to end-stage liver cirrhosis.In recent years, the collective research efforts on the cellular and molecular mechanisms underlying this pathogenic condition have uncovered important regulatory roles for microRNAs (miRs) and autophagy signaling.In particular, miR-mediated silencing of target gene expression has been shown to regulate activation of the hepatic stellate cells (HSCs) , which are the main source of the aberrantly synthesized and deposited extracellular matrix proteins.While several specific miRs have been identified and functionally characterized under conditions of liver fibrosis, such as miR-29b and its effects on type I collagen and TGFβ signaling, the entire panel of miRs and their contribution to the pathogenic process remains to be fully elucidated.Autophagy signaling has also been shown to regulate HSC activation.In particular, autophagy signaling stimulates the release of retinol ester and triglyceride containing lipid droplets from quiescent HSCs, and the energy generated from these fatty acids' breakdown causes HSC activation.In this review, the current knowledge on each of these newly recognized pathogenic mechanisms is summarized.By expanding our knowledge of the fibrogenesis-related processes involving miRs and/or autophagy signaling pathways/factors, effective molecular biomarkers may be identified to improve diagnosis, and novel therapeutic strategies may be developed for clinical applications.