Objective To investigate the effects of microRNA (miR)-30a-regulated MAPK pathway on the formation of intercalation, inflammatory factors and vasoconstriction in a rat model of aortic coarctation.   Methods Fifty SD rats were selected to establish the rat model of aortic coarctation, and were randomly divided into control group, model group, miR-NC group, miR-30a group and miR-30a inhibitor group, 10 rats in each group. Histopathological changes in the aortic tissue and changes in the elastic fibers and collagen fibers of the aortic mesothelium were observed; The expression of miR-30a, systolic blood pressure before and after the intervention and the expression of serum inflammatory factors in each group were measured by PCR, tail artery manometry and ELISA; Matrix metalloproteinase (MMP)-6, MMP-2 protein expression and MAPK pathway were measured by Western blotting in each group. The expression of MMP-6, MMP-2 and MAPK pathway related proteins were measured by Western blotting.   Results The miR-30a inhibitor group improved the degree of vessel wall tearing and disorganized internal arterial wall arrangement; The miR-30a group improved vascular remodeling; miR-30a expression was higher in the model group compared with the control group, and lower in the miR-30a group and miR-30a inhibitor group compared with the miR-NC group, P<0.05; Before the intervention, the difference in systolic blood pressure between the groups compared was not statistically significant, P> 0.05; Compared with the control group, systolic blood pressure was higher in the model group, higher expression in the miR-30a group and lower expression in the miR-30a inhibitor group compared with the miR-NC group, P< 0.05; compared with the control group, tumor necrosis factor(TNF)-α, interleukin (IL)-6, IL-1β expression was higher in the model group, higher expression in the miR-30a group compared with the miR-NC group, lower expression in the miR-30a inhibitor group, P< 0.05; higher expression of TNF-α, MMP-6, MMP-2, Ras, Raf, P38MAPK, ERK1/2 proteins in the model group compared with the control group, higher expression in the miR-30a group compared with the miR-NC group, lower expression in the miR-30a inhibitor group, P<0.05.   Conclusion MiR-30a is involved in the process of aortic coarctation formation, inflammatory response, and regulation of aortic coarctation vascular remodeling, possibly through regulation of the MAPK signaling pathway.