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dc.contributor.otherProducción Científica UCH 2021-
dc.contributor.otherUCH. Departamento de Producción y Sanidad Animal, Salud Pública Veterinaria y Ciencia y Tecnología de los Alimentos-
dc.contributor.otherUCH. Departamento de Ciencias Biomédicas-
dc.creatorGómez Roda, Olga.-
dc.creatorPerini Villanueva, Giuliana.-
dc.creatorYuste Rivero, Andrea.-
dc.creatorRodríguez Navarro, José Antonio.-
dc.creatorPoch Jiménez, Enric.-
dc.creatorBejarano Fernández, Eloy.-
dc.date2021-
dc.date.accessioned2022-04-09T04:00:59Z-
dc.date.available2022-04-09T04:00:59Z-
dc.date.issued2021-12-23-
dc.identifier.citationGómez, O., Perini-Villanueva, G., Yuste, A., Rodríguez-Navarro, J. A., Poch, E. & Bejarano, E. (2021). Autophagy and glycative stress: a bittersweet relationship in neurodegeneration. Frontiers in Cell and Developmental Biology, vol. 9, art. 790479 (23 dec.). DOI: https://doi.org/10.3389/fcell.2021.790479-
dc.identifier.issn2296-634X (Electrónico)-
dc.identifier.urihttp://hdl.handle.net/10637/13646-
dc.descriptionEste artículo se encuentra disponible en la siguiente URL: https://www.frontiersin.org/articles/10.3389/fcell.2021.790479/full-
dc.description.abstractAutophagy is a fine-tuned proteolytic pathway that moves dysfunctional/aged cellular components into the lysosomal compartment for degradation. Over the last 3 decades, global research has provided evidence for the protective role of autophagy in different brain cell components. Autophagic capacities decline with age, which contributes to the accumulation of obsolete/damaged organelles and proteins and, ultimately, leads to cellular aging in brain tissues. It is thus well-accepted that autophagy plays an essential role in brain homeostasis, and malfunction of this catabolic system is associated with major neurodegenerative disorders. Autophagy function can be modulated by different types of stress, including glycative stress. Glycative stress is defined as a cellular status with abnormal and accelerated accumulation of advanced glycation end products (AGEs). It occurs in hyperglycemic states, both through the consumption of high-sugar diets or under metabolic conditions such as diabetes. In recent years, glycative stress has gained attention for its adverse impact on brain pathology. This is because glycative stress stimulates insoluble, proteinaceous aggregation that is linked to the malfunction of different neuropathological proteins. Despite the emergence of new literature suggesting that autophagy plays a major role in fighting glycation-derived damage by removing cytosolic AGEs, excessive glycative stress might also negatively impact autophagic function. In this mini-review, we provide insight on the status of present knowledge regarding the role of autophagy in brain physiology and pathophysiology, with an emphasis on the cytoprotective role of autophagic function to ameliorate the adverse effects of glycation-derived damage in neurons, glia, and neuron-glia interactions.-
dc.formatapplication/pdf-
dc.language.isoen-
dc.language.isoes-
dc.publisherFrontiers Media-
dc.relationEste trabajo de investigación fue financiado por el RYC 2018-024434-I, por el MINECO PID 2020-119466RB-I00, FUSP-PPC-19-B53C4C64, MINECO SAF 2016 78666-R, ISCIII CP19 010, PID 2020-113014RB-I00 funded by MCIN/AEI/10.13039/501100011033 y FUSP-PPC-19-28A751CC.-
dc.relationUCH. Financiación Nacional-
dc.relation.ispartofFrontiers in Cell and Developmental Biology, vol. 9-
dc.rightshttp://creativecommons.org/licenses/by/4.0/deed.es-
dc.subjectSistema nervioso - Degeneración.-
dc.subjectSystem nervous - Degeneration.-
dc.subjectOxidation, Physiological.-
dc.subjectOxidación biológica.-
dc.subjectDevelopmental biology.-
dc.subjectCells - Aging.-
dc.subjectCélulas - Envejecimiento.-
dc.subjectBiología del desarrollo.-
dc.titleAutophagy and glycative stress : a bittersweet relationship in neurodegeneration-
dc.typeArtículo-
dc.identifier.doihttps://doi.org/10.3389/fcell.2021.790479-
dc.relation.projectIDRYC 2018-024434-I-
dc.relation.projectIDPID 2020-119466RB-I00-
dc.relation.projectIDFUSP-PPC-19-B53C4C64-
dc.relation.projectIDSAF 2016 78666-R-
dc.relation.projectIDCP19 010-
dc.relation.projectIDPID 2020-113014RB-I00-
dc.relation.projectIDMCIN/AEI/10.13039/501100011033-
dc.relation.projectIDFUSP-PPC-19-28A751CC-
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