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dc.contributor.authorHou, Xines
dc.contributor.authorXiao, Haitaoes
dc.contributor.authorZhang, Yanhonges
dc.contributor.authorZeng, Xixies
dc.contributor.authorHuang, Mengjunes
dc.contributor.authorChen, Xiaoyunes
dc.contributor.authorBirnbaumer, Lutzes
dc.contributor.authorLiao, Yanhonges
dc.date.accessioned2019-09-04T18:10:20Z-
dc.date.available2019-09-04T18:10:20Z-
dc.date.issued2018-
dc.identifier.citationHou X, Xiao H, Zhang Y, et al. Transient receptor potential channel 6 knockdown prevents apoptosis of renal tubular epithelial cells upon oxidative stress via autophagy activation. Cell Death & Disease. 2018;9(10):1-15. doi:10.1038/s41419-018-1052-5 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8686es
dc.identifier.issn2041-4889-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8686-
dc.description.abstractAbstract: Reactive oxygen species (ROS) are generated under various pathological conditions such as renal ischemia/reperfusion (I/R) injury and provoke damage to multiple cellular organelles and processes. Overproduction of ROS causes oxidative stress and contributes to damages of renal proximal tubular cells (PTC), which are the main cause of the pathogenesis of renal I/R injury. Autophagy is a dynamic process that removes long-lived proteins and damaged organelles via lysosome-mediated degradation, which has an antioxidant effect that relieves oxidative stress. The canonical transient receptor potential channel 6 (TRPC6), a nonselective cation channel that allows passage of Ca2+, plays an important role in renal disease. Yet, the relationship between TRPC6 and autophagy, as well as their functions in renal oxidative stress injury, remains unclear. In this study, we found that oxidative stress triggered TRPC6-dependent Ca2+ influx in PTC to inhibit autophagy, thereby rendering cells more susceptible to death. We also demonstrated that TRPC6 knockout (TRPC6-/-) or inhibition by SAR7334, a TRPC6-selective inhibitor, increased autophagic flux and mitigated oxidative stress-induced apoptosis of PTC. The protective effects of TRPC6 ablation were prevented by autophagy inhibitors Chloroquine and Bafilomycin A1. Moreover, this study also shows that TRPC6 blockage promotes autophagic flux via inhibiting the PI3K/Akt/mTOR and ERK1/2 signaling pathways. This is the first evidence showing that TRPC6-mediated Ca2+ influx plays a novel role in suppressing cytoprotective autophagy triggered by oxidative stress in PTC, and it may become a novel therapeutic target for the treatment of renal oxidative stress injury in the future.es
dc.formatapplication/pdf-
dc.language.isoenges
dc.publisherNature Publishing Groupes
dc.rightsAcceso Abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourceCell Death & Disease. 2018;9(10):1-15es
dc.subjectRIÑONes
dc.subjectESTRES OXIDATIVOes
dc.subjectAPOPTOSISes
dc.subjectCELULAS EPITELIALESes
dc.subjectINSUFICIENCIA RENALes
dc.titleTransient receptor potential channel 6 knockdown prevents apoptosis of renal tubular epithelial cells upon oxidative stress via autophagy activationes
dc.typeArtículoes
dc.identifier.doi10.1038/s41419-018-1052-5-
dc.identifier.pmid30282964-
uca.disciplinaMEDICINA-
uca.issnrd1es
uca.affiliationFil: Hou, Xin. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Hou, Xin. Hebei University of Engineering. Affiliated Hospital. Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Xiao, Haitao. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Xiao, Haitao. Huazhong University of Science and Technology. Tongji Medical College. Key Laboratory of Neurological Diseases of Ministry of Education; Chinaes
uca.affiliationFil: Zhang, Yanhong. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Zhang, Yanhong. Huazhong University of Science and Technology. Tongji Medical College. Key Laboratory of Neurological Diseases of Ministry of Education; Chinaes
uca.affiliationFil: Zeng, Xixi. Huazhong. University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Zeng, Xixi. Huazhong. University of Science and Technology. Tongji Medical College. Key Laboratory of Neurological Diseases of Ministry of Education; Chinaes
uca.affiliationFil: Huang, Mengjun. University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Huang, Mengjun. University of Science and Technology. Tongji Medical College. Key Laboratory of Neurological Diseases of Ministry of Education; Chinaes
uca.affiliationFil: Chen, Xiaoyun. First Hospital of Wuhan. Department of Pathology; Chinaes
uca.affiliationFil: Birnbaumer, Lutz. Research Triangle Park. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidoses
uca.affiliationFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Liao, Yanhong. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Liao, Yanhong. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.versionpublishedVersiones
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.languageiso639-1en-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Función y Farmacología de Canales Iónicos-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptFacultad de Ciencias Médicas-
crisitem.author.orcid0000-0002-0775-8661-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgPontificia Universidad Católica Argentina-
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