Please use this identifier to cite or link to this item: https://hdl.handle.net/11000/6893
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dc.contributor.authorBelló Pérez, Melissa-
dc.contributor.authorSola, Isabel-
dc.contributor.authorNovoa, Beatriz-
dc.contributor.authorDaniel J., Klionsky-
dc.contributor.authorFalcó, Alberto-
dc.date.accessioned2021-01-14T08:00:56Z-
dc.date.available2021-01-14T08:00:56Z-
dc.date.created2020-07-01-
dc.date.issued2021-01-14-
dc.identifier.issn2073-4409-
dc.identifier.urihttp://hdl.handle.net/11000/6893-
dc.description.abstractThe SARS-CoV-2 pandemic necessitates a review of the molecular mechanisms underlying cellular infection by coronaviruses, in order to identify potential therapeutic targets against the associated new disease (COVID-19). Previous studies on its counterparts prove a complex and concomitant interaction between coronaviruses and autophagy. The precise manipulation of this pathway allows these viruses to exploit the autophagy molecular machinery while avoiding its protective apoptotic drift and cellular innate immune responses. In turn, the maneuverability margins of such hijacking appear to be so narrow that the modulation of the autophagy, regardless of whether using inducers or inhibitors (many of which are FDA-approved for the treatment of other diseases), is usually detrimental to viral replication, including SARS-CoV-2. Recent discoveries indicate that these interactions stretch into the still poorly explored noncanonical autophagy pathway, which might play a substantial role in coronavirus replication. Still, some potential therapeutic targets within this pathway, such as RAB9 and its interacting proteins, look promising considering current knowledge. Thus, the combinatory treatment of COVID-19 with drugs affecting both canonical and noncanonical autophagy pathways may be a turning point in the fight against this and other viral infections, which may also imply beneficial prospects of long-term protectiones
dc.description.sponsorshipThis research was funded by the FEDER/Spanish Ministry of Science and Innovation – State Agency of Research, grant number RTI2018-101969-J-I00-
dc.description.sponsorshipCSIC and Ministry of Science and Innovation of Spain (BIO2016-75549-R AEI/FEDER, UE; PIE Ref. 202020E079; PIE CSIC Ref. 202020E043),-
dc.description.sponsorshipEuropean Commission, H2020-SC1-2019 (Improved Vaccination Strategies for Older Adults, ISOLDA_Ref. 848166)-
dc.description.sponsorshipand U.S. National Institutes of Health (NIH) (2P01AI060699, 0258-3413/HHSN266200700010C and GM131919). M.B.-P. received a contract from NIH.-
dc.formatapplication/pdfes
dc.format.extent18es
dc.language.isoenges
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectantivirales
dc.subjectautophagyes
dc.subjectcanonical autophagyes
dc.subjectcoronaviruses
dc.subjectCOVID-19es
dc.subjectnoncanonical autophagyes
dc.subjectSARS-CoV-2es
dc.titleCanonical and Noncanonical Autophagy as Potential Targets for COVID-19es
dc.typeinfo:eu-repo/semantics/articlees
dc.contributor.instituteInstituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elchees
dc.identifier.doi10.3390/cells9071619-
dc.relation.publisherversionhttps://doi.org/10.3390/cells9071619-
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Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche


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