About: Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal

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About: Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal
Creator	Romero, F Barcia, J Bonet-Ponce, L Flores-Bellver, M Galindo, M Garcia-Verdugo, J Jordan, J Martinez-Gil, N Saez-Atienzar, S Sancho-Pelluz, J
Source	Medline; PMC
abstract	Retinal pigment epithelium has a crucial role in the physiology and pathophysiology of the retina due to its location and metabolism. Oxidative damage has been demonstrated as a pathogenic mechanism in several retinal diseases, and reactive oxygen species are certainly important by-products of ethanol (EtOH) metabolism. Autophagy has been shown to exert a protective effect in different cellular and animal models. Thus, in our model, EtOH treatment increases autophagy flux, in a concentration-dependent manner. Mitochondrial morphology seems to be clearly altered under EtOH exposure, leading to an apparent increase in mitochondrial fission. An increase in 2′,7′-dichlorofluorescein fluorescence and accumulation of lipid peroxidation products, such as 4-hydroxy-nonenal (4-HNE), among others were confirmed. The characterization of these structures confirmed their nature as aggresomes. Hence, autophagy seems to have a cytoprotective role in ARPE-19 cells under EtOH damage, by degrading fragmented mitochondria and 4-HNE aggresomes. Herein, we describe the central implication of autophagy in human retinal pigment epithelial cells upon oxidative stress induced by EtOH, with possible implications for other conditions and diseases.
has issue date	2014-07-17(xsd:dateTime)
bibo:doi	10.1038/cddis.2014.288
bibo:pmid	25032851
has license	cc-by-nc-nd
sha1sum (hex)	fd269eab4eea4042324ce40b35674a7b2c0773ad
schema:url	https://doi.org/10.1038/cddis.2014.288
resource representing a document's title	Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal
has PubMed Central identifier	PMC4123082
has PubMed identifier	25032851
schema:publication	Cell Death Dis
resource representing a document's body	covid:fd269eab4eea4042324ce40b35674a7b2c0773ad#body_text
is schema:about of	named entity 'retinal pigment epithelial' named entity 'cellular' named entity 'accumulation' named entity 'human' named entity 'Autophagy' named entity 'ETHANOL' named entity 'OUR' named entity 'DISEASES' named entity 'CENTRAL' named entity 'HAVE' named entity 'CELLS' named entity 'INCREASE' named entity 'THESE' named entity 'DICHLOROFLUORESCEIN' named entity 'CONCENTRATION' named entity 'THEIR' named entity 'PHYSIOLOGY' named entity 'LEADING' named entity 'APPARENT' named entity 'MITOCHONDRIAL MORPHOLOGY' named entity 'Autophagy' named entity 'products' named entity 'mechanism' named entity 'cells' named entity 'apparent' named entity 'structures' named entity 'implications' named entity '4-HNE' named entity '4-HNE' named entity 'metabolism' named entity 'metabolism' named entity 'oxidative stress' named entity 'retina' named entity 'cytoprotective' named entity 'morphology' named entity 'Oxidative damage' named entity 'mitochondrial fission' named entity 'EtOH' named entity 'mitochondria' named entity 'lipid peroxidation' named entity 'Autophagy' named entity 'retinal pigment epithelial' named entity 'mitochondria' named entity 'EtOH' named entity 'Misfolded' named entity 'neurodegenerative diseases' named entity 'autophagosome' named entity 'incubation' named entity 'MTT assay' named entity 'EtOH' named entity 'neurodegeneration' named entity 'autophagic' named entity 'EtOH' named entity 'adaptor molecule' named entity 'Japan' named entity 'cell death' named entity 'mitochondria' named entity 'autophagosome' named entity 'Electron microscopy' named entity 'morphology' named entity 'Thermo Scientific' named entity 'Lipid peroxidation' named entity 'nucleoli' named entity 'oxidative stress' named entity 'EtOH' named entity 'EtOH' named entity 'autophagosome' named entity 'aggresomes' named entity 'toxicity' named entity 'ROS' named entity 'toxicity' named entity 'Wetzlar'

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