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Fig. 2 | Molecular Medicine

Fig. 2

From: MicroRNA-296: a promising target in the pathogenesis of atherosclerosis?

Fig. 2

The roles of miR-296 and their target genes in atherosclerosis. MiR-296 promotes angiogenesis via reducing the levels of HGS and then elevating VEGFR2 and PDGFR-β, and simultaneously reducing the expression levels of DLL4 and Notch1 (the mechanism is not clear). MiR-296 promotes the inflammatory response. MiR-296 targeted inhibition of NumbL and subsequent NF-κB activation; miR-296 represses IKBKE and then enhances NLRP3 inflammasome; miR-296 inhibits the expression of STAT5A and then represses SOCS-2 and promotes M1 macrophage polarization; miR-296 directly suppresses Scrib and subsequently promotes M1 macrophage polarization and ROS generation, these entire can promote inflammation. MiR-296 could repress ICAM-1 and CX3CR1 and then inhibit monocyte adhesion. MiR-296 promotes MDR1 expression and subsequent intestinal cholesterol reabsorption. MiR-296 inhibits WNK4 expression and downregulates salt-sensitive hypertension. MiR-296 suppresses p53, p21WAF1, p27 and PTEN expression and then promotes cells proliferation. MiR-296 targeted inhibition of NGFR and caspase-8 promotes cell apoptosis. The black word: Direct target of miR-296, the red word: Expression increased, the green word: Expression decreased. : promote, : inhibit

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