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Neutrophil extracellular traps target senescent vasculature for tissue remodeling in retinopathy

Title: Neutrophil extracellular traps target senescent vasculature for tissue remodeling in retinopathy
Authors: Binet, François; Cagnone, Gael; Crespo-Garcia, Sergio; Hata, Masayuki; Neault, Mathieu; Dejda, Agnieszka; Wilson, Ariel M.; Buscarlet, Manuel; Mawambo, Gaelle Tagne; Howard, Joel P.; Diaz-Marin, Roberto; Parinot, Celia; Guber, Vera; Pilon, Frédérique; Juneau, Rachel; Laflamme, Rémi; Sawchyn, Christina; Boulay, Karine; Leclerc, Severine; Abu-Thuraia, Afnan; Côté, Jean-François; Andelfinger, Gregor; Rezende, Flavio A.; Sennlaub, Florian; Joyal, Jean-Sébastien; Mallette, Frédérick A.; Sapieha, Przemyslaw
Contributors: Burroughs Wellcome Fund; Heart and Stroke Foundation of Canada; Canadian Diabetes Association; Canadian Institutes of Health Research; Banque Nationale Research Excellence Chair in Cardiovascular Genetics; Natural Sciences and Engineering Research Council of Canada; Fonds de Recherche du Québec - Santé; Mitacs
Source: Science ; volume 369, issue 6506 ; ISSN 0036-8075 1095-9203
Publisher Information: American Association for the Advancement of Science (AAAS)
Publication Year: 2020
Description: Remodeling senescent blood vessels The retina is a thin layer of nervous tissue at the back of the eye that transforms light into neuronal signals. The retina is essential for vision and is supported by networks of blood vessels. In diabetic retinopathy, a common cause of vision loss, these microvessels degenerate and regrow in an aberrant manner. Such degeneration and regrowth can compromise the functioning of retinal nerve cells. Binet et al. observed that, after rapid proliferation, vascular endothelial cells in diseased blood vessels engaged molecular pathways linked to cellular senescence (see the Perspective by Podrez and Byzova). Senescent vascular units summoned an inflammatory response in which neutrophils extruded neutrophil extracellular traps onto diseased vessels to remodel them. This endogenous repair mechanism promoted the elimination of senescent blood vessels and could lead to beneficial vascular remodeling. Science , this issue p. eaay5356 ; see also p. 919
Document Type: article in journal/newspaper
Language: English
DOI: 10.1126/science.aay5356
Availability: https://doi.org/10.1126/science.aay5356; https://syndication.highwire.org/content/doi/10.1126/science.aay5356; https://www.science.org/doi/pdf/10.1126/science.aay5356
Accession Number: edsbas.4CA15A50
Database: BASE