Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Mar 26;24:12. doi: 10.1186/s10020-018-0012-y

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

PMC Copyright notice

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

Inline graphic — 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