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Activated hepatic stellate cells (aHSCs) play a key role in liver fibrosis. During the regression of fibrosis, aHSCs are transformed into inactivated cells (iHSCs), which are quiescent lipid-containing cells and express higher levels of lipid-related genes, such as peroxisome proliferators-activated receptors gamma (PPAR&#947;). Here, we investigated the role of <i>MicroRNA29a (Mir29a)</i> in the resolution of liver fibrosis. <i>Mir29a</i> and lipid-related genes were up-regulated after the recovery of CCl₄-induced liver fibrosis in mice. PPAR&#947; agonist rosiglitazone (RSG) promoted de-differentiation of aHSCs to iHSCs and up-regulated <i>MIR29a</i> expression in a human HSC cell line LX-2. <i>MIR29a</i> mimics in vitro promoted the expression of lipid-related genes, while decreased the expression of fibrosis-related genes. <i>MIR29a</i> inhibitor showed the reverse effects. ATPase H⁺ transporting V1 subunit C1 (Atp6v1c1) was increased in liver fibrosis, while down-regulated after the recovery in mice, and negatively regulated by <i>MIR29a</i> in LX-2 cells. Knockdown of ATP6V1C1 by siRNA decreased alpha-smooth muscle actin (&#945;-<i>SMA</i>) and increased lipid-related genes expression. Simultaneous addition of <i>MIR29a</i> mimics and <i>ATP6V1C1</i> siRNA further increased RSG promoted expression of lipid-related proteins in vitro. Collectively, <i>MIR29a</i> plays an important role during the trans-differentiation of aHSCs in the resolution of liver fibrosis, in part, through regulation of <i>ATP6V1C1</i>.