Cardiac fibrosis is an essential pathological process in pressure overload (PO)induced heart failure. Recently, myocyte-fibroblast communication is proven to be critical in heart failure, in which, pathological growth of cardiomyocytes (CMs) may promote fibrosis via miRNAs-containing exosomes (Exos). Peli1 regulates the activation of NF-κB and AP-1, which has been demonstrated to engage in miRNA transcription in cardiomyocytes. Therefore, we hypothesized that Peli1 in CMs regulates the activation of cardiac fibroblasts (CFs) through an exosomal miRNAmediated paracrine mechanism, thereby promoting cardiac fibrosis. We found that CM-conditional deletion of Peli1 improved PO-induced cardiac fibrosis. Moreover, Exos from mechanical stretch (MS)-induced WT CMs (WT MS-Exos) promote activation of CFs, Peli1 −/− MS-Exos reversed it. Furthermore, miRNA microarray and qPCR analysis showed that miR-494-3p was increased in WT MS-Exos while being down regulated in Peli1 −/− MS-Exos. Mechanistically, Peli1 promoted miR-494-3p

Background: Age-related macular degeneration (AMD) is one of the leading causes of permanent visual impairment in the elderly. Blue light (BL) has been reported to cause retinal damage and contribute to the onset and development of severe AMD. N-retinylidene-N-retinylethanolamine (A2E), a lipofuscin fluorophore, accumulates with ageing in the retinal pigment epithelium (RPE) cells. Once exposed to BL, A2E easily oxidizes to A2E-epoxides, causing oxidative-stress injury to the retina. Lipoxin A4 (LXA4), an endogenous anti-antioxidant lipid, plays a key role in multiple organs by binding to the formyl-peptide receptor-like 1 (FPRL1). This study examined the protective effects of LXA4 on oxidative-stress injury induced by BL exposure, and clarified the underlying mechanisms in cultured RPE cells and Balb-c mice.Methods: LXA4 diluent was orally administered to mice before retinal degeneration was established.Optical coherence tomography, retinal histology, and RPE cell injury were assessed.Results: LXA4 administration significantly ameliorated retinal damage as evidenced by the thicknesses of the retinal layers and the tight junctions of RPE cells in vivo. LXA4 inhibited BL-induced reactive oxygen species (ROS) production, reduced tight junctions, and the death of A2E-laden RPE cells. LXA4 also potently increased the expression of haem oxygenase-1 (HO1) and NAD(P)H quinone oxidoreductase 1 (NQO1), probably by decreasing the association between nuclear factor erythroid 2-related factor 2 (NRF2) and Kelch-like ECH (Epichlorohydrin) -associated protein 1 (Keap1), and ameliorating NRF2 nuclear translocation and the antioxidant response element (ARE) deoxyribonucleic acid (DNA) binding activity.Conclusions: Our results showed that LXA4 ameliorated retinal degeneration, and should be considered in the prevention and treatment of AMD.

Withdrawn: “Prostaglandin E2 promotes retinal microvascular endothelial cell‐derived miR‐423‐5p‐containing extracellular vesicles inducing Müller cell activation in diabetic retinopathy”, by Xiaolu Wang, Yanqiu Liu, Qian Yang, Yishun Shu, Chao Sun, Li Yin, Jian Zou, Pengfei Zhan, Yangningzhi Wang, Meili Wu, Xusheng Yang, Jiping Cai, Yong Yao, and Tianhua Xie, Traffic. The above article, published as accepted article online on 12 February 2022 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1111/tra.12837) has been withdrawn by agreement between the authors and the journal's Editors in Chief, Drs. Eric Chevet, Antonella De Matteis, Eeva‐Liisa Eskelinen, Hesso Farhan, and John Wiley & Sons Ltd.The withdrawal was agreed upon request by the authors.