Objective: Present study focused on the influence of lncRNA MALAT1 on coronary atherosclerotic heart disease (CAD) by regulating miR-15b-5p/ MAPK1 and mTOR signaling pathway. Method: Differentially expressed genes and activated pathway were investigated through bioinformatics analysis. QRT-PCR was conducted to verify expression of MALAT1 , miR-15b-5p and MAPK1 in CAD blood samples and endothelial progenitor cells (EPCs). In addition, the interactions among MALAT1 , miR-15b-5p and MAPK1 were revealed by Luciferase reporter assay. Cell autophagy of EPCs was examined by Cyto-ID Autophagy Detection Kit and transmission electron microscope. MTT assay and flow cytometry were carried out to assess cell viability and apoptosis in different interference conditions. Western blot was performed to testify the expression of pERK1/2 (MAPK1), phosphorylated mTOR, ATG1 and LC3-II. Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were detected by qRT-PCR. Finally, the effect of lncRNA MALAT1 on cell autophagy and atherogenesis was tested in vivo . Results: MALAT1 was overexpressed in CAD blood samples and EPCs. Knockdown of MALAT1 and MAPK1 promoted cell viability, autophagy and further suppressed the development of CAD. Antago MALAT1 protects mice against atherosclerosis. Conclusion: LncRNA MALAT1 inhibited EPCs autophagy and increased cell viability while repressed apoptosis of CAD via activating mTOR signaling pathway.

The results indicated that Grb1 can exert anti-HF function by inhibiting cardiomyocyte autophagy of rats through regulation of Rho/ROCK and PI3K/mTOR pathways.

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coronary artery bypass graft (cABG) is one of the primary methods of treating coronary heart disease (cHd); however, vein graft restenosis is a major limiting factor of the effectiveness of cABG. Emerging evidence has indicated that miR-423 is associated with vascular diseases. Additionally, upregulation of a disintegrin and metalloproteinase with thrombospondin motifs-7 (AdAMTS-7) contributes to neointima formation by promoting the proliferation and migration of vascular smooth muscle cells and inhibiting the proliferation and migration of endothelial cells. The aim of the present study was to examine the effects of miR-423 target, AdAMTS-7, on regulating vein graft disease and identify novel biomarkers for use in therapy of vein graft failure (VGF). Aberrant expression of miR-423 in plasma of patients with CHD prior to and following CABG confirms that miR-423 may be a suitable target for preventing VGF. Furthermore, a dual-luciferase reporter gene assay indicated that miR-423 directly interacted with AdAMTS-7 and suppressed its expression. Ectopic expression of miR-423 suppressed AdAMTS-7, resulting in decreased proliferation and migration rates of human umbilical vein smooth muscle cells by targeting AdAMTS-7, but resulted in increased proliferation and migration of human umbilical vein endothelial cells in vitro. Overexpression of miR-423 also enhanced re-endothelialization and decreased neointimal formation in a rat vein graft model. In conclusion, the results of the present study demonstrated that the miR-423/AdAMTS-7 axis may possess potential clinical value for the prevention and treatment of restenosis in patients with cHd following cABG.