Key points are not available for this paper at this time.
(Molecular Therapy 25, 1279–1294; June 2017) This article has been retracted at the request of the editors. The editorial office received emails from the corresponding authors of this article requesting that this article be corrected due to image duplication in Figure 3D initially identified in a PubPeer post (https://pubpeer.com/publications/27DB27049037B0035A83F35E244A8B). Image analysis conducted by the editorial office indicated inappropriate post processing of images in Figure 3D, image duplication within Figures 3D and 5D, and image recycling between Figure 5D of the Molecular Therapy article and Figure 3B of an article in Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (Zheng et al., 2018, Biochim. Biophys. Acta Mol. Basis Dis. 1864, 374–386. https://doi.org/10.1016/j.bbadis.2017.10.021). While some original data was provided in response to the editors' request, discrepancies exist between the data provided and the published data. Given these issues, the editors have lost faith in the findings presented in the article. This reuse (and in part misrepresentation) of data without appropriate attribution represents a severe abuse of the scientific publishing system. Exosome-Mediated miR-155 Transfer from Smooth Muscle Cells to Endothelial Cells Induces Endothelial Injury and Promotes AtherosclerosisZheng et al.Molecular TherapyMarch 28, 2017In BriefZheng et al. show that KLF5 exerts a pro-atherosclerotic effect by regulating the secretion miR-155. miR-155-rich exosomes from KLF5-overexpressing VSMCs are taken up by ECs. miR-155-rich exosomes inhibit the proliferation and migration of ECs and impair endothelial cell barrier function by suppressing the expression of tight junction proteins. Targeting miR-155 might represent a therapeutic strategy in atherosclerosis. Full-Text PDF Open Archive
Zheng et al. (Fri,) studied this question.