Autophagy : supporting cellular and organismal homeostasis by self-eating

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dc.contributor University of Helsinki, Molecular and Integrative Biosciences Research Programme en Eskelinen, Eeva-Liisa 2020-04-04T01:59:37Z 2021-06-16T02:46:11Z 2019-06
dc.identifier.citation Eskelinen , E-L 2019 , ' Autophagy : supporting cellular and organismal homeostasis by self-eating ' , International Journal of Biochemistry & Cell Biology , vol. 111 , pp. 1-10 . en
dc.identifier.issn 1357-2725
dc.identifier.other PURE: 123696812
dc.identifier.other PURE UUID: 020fd29b-f635-43e6-8be6-4ec6d5e5e807
dc.identifier.other WOS: 000470192000001
dc.identifier.other ORCID: /0000-0003-0006-7785/work/60404189
dc.description.abstract Autophagy is a conserved catabolic process that delivers cytoplasmic components and organelles to lysosomes for degradation and recycling. This pathway serves to degrade nonfunctional organelles and aggregate-prone proteins, as well as to produce substrates for energy production and biosynthesis. Autophagy is especially important for the maintenance of stem cells, and for the survival and homeostasis of post-mitotic cells like neurons. Functional autophagy promotes longevity in several model organisms. Autophagy regulates immunity and inflammation at several levels and has both anti- and pro-tumorigenic roles in cancer. This review provides a concise overview of autophagy and its importance in cellular and organismal homeostasis, with emphasis on aging, stem cells, neuronal cells, immunity, inflammation, and cancer. en
dc.format.extent 10
dc.language.iso eng
dc.relation.ispartof International Journal of Biochemistry & Cell Biology
dc.rights en
dc.subject 1182 Biochemistry, cell and molecular biology en
dc.subject autophagy en
dc.subject aging en
dc.subject stem cells en
dc.subject immunity en
dc.subject Inflammation en
dc.subject neurodegeneration en
dc.subject cancer en
dc.title Autophagy : supporting cellular and organismal homeostasis by self-eating en
dc.type Review Article
dc.type.uri info:eu-repo/semantics/other

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