Number of the records: 1  

Mitochondrial respiration supports autophagy to provide stress resistance during quiescence

  1. 1.
    SYSNO ASEP0557875
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleMitochondrial respiration supports autophagy to provide stress resistance during quiescence
    Author(s) Magalhaes-Novais, Silvia (BTO-N) ORCID
    Blecha, Jan (BTO-N)
    Naraine, Ravindra (BTO-N)
    Mikesova, Jana (BTO-N)
    Abaffy, Pavel (BTO-N)
    Pecinová, Alena (FGU-C) RID, ORCID, SAI
    Miloševič, Mirko (BTO-N)
    Bohuslavová, Romana (BTO-N) RID
    Procházka, Jan (UMG-J) ORCID
    Khan, S. (BE)
    Novotná, Eliška (BTO-N)
    Šindelka, Radek (BTO-N) RID
    Machan, R. (BE)
    Dewerchin, M. (BE)
    Vlčák, Erik (UMG-J)
    Kalucka, J. (BE)
    Štemberková-Hubáčková, Soňa (BTO-N)
    Benda, A. (CZ)
    Goveia, J. (BE)
    Mráček, Tomáš (FGU-C) RID, ORCID
    Bařinka, Cyril (BTO-N) RID, ORCID
    Carmeliet, P. (BE)
    Neužil, Jiří (BTO-N) RID
    Rohlenová, Kateřina (BTO-N) ORCID, RID
    Rohlena, Jakub (BTO-N) RID, ORCID
    Number of authors25
    Source TitleAutophagy. - : Taylor & Francis - ISSN 1554-8627
    Roč. 18, č. 10 (2022), s. 2409-2426
    Number of pages19 s.
    Languageeng - English
    CountryUS - United States
    KeywordsATG4B ; cell death ; biosynthesis ; electron transport chain
    Subject RIVEB - Genetics ; Molecular Biology
    OECD categoryCell biology
    R&D ProjectsGA20-18513S GA ČR - Czech Science Foundation (CSF)
    GA17-24441S GA ČR - Czech Science Foundation (CSF)
    GA20-05942S GA ČR - Czech Science Foundation (CSF)
    GA18-02550S GA ČR - Czech Science Foundation (CSF)
    GX21-04607X GA ČR - Czech Science Foundation (CSF)
    GA22-34507S GA ČR - Czech Science Foundation (CSF)
    NV17-30138A GA MZd - Ministry of Health (MZ)
    NV17-32727A GA MZd - Ministry of Health (MZ)
    NU21-03-00545 GA MZd - Ministry of Health (MZ)
    NU20J-02-00035 GA MZd - Ministry of Health (MZ)
    LM2018129 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    LM2015040 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    LM2018126 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    EF18_046/0015861 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    EF16_013/0001775 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    EF18_046/0016045 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Research InfrastructureCzech-BioImaging II - 90129 - Ústav molekulární genetiky AV ČR, v. v. i.
    CCP II - 90126 - Ústav molekulární genetiky AV ČR, v. v. i.
    Method of publishingOpen access
    Institutional supportBTO-N - RVO:86652036 ; UMG-J - RVO:68378050 ; FGU-C - RVO:67985823
    UT WOS000766134900001
    EID SCOPUS85126384039
    DOI10.1080/15548627.2022.2038898
    AnnotationMitochondrial oxidative phosphorylation (OXPHOS) generates ATP, but OXPHOS also supports biosynthesis during proliferation. In contrast, the role of OXPHOS during quiescence, beyond ATP production, is not well understood. Using mouse models of inducible OXPHOS deficiency in all cell types or specifically in the vascular endothelium that negligibly relies on OXPHOS-derived ATP, we show that selectively during quiescence OXPHOS provides oxidative stress resistance by supporting macroautophagy/autophagy. Mechanistically, OXPHOS constitutively generates low levels of endogenous ROS that induce autophagy via attenuation of ATG4B activity, which provides protection from ROS insult. Physiologically, the OXPHOS-autophagy system (i) protects healthy tissue from toxicity of ROS-based anticancer therapy, and (ii) provides ROS resistance in the endothelium, ameliorating systemic LPS-induced inflammation as well as inflammatory bowel disease. Hence, cells acquired mitochondria during evolution to profit from oxidative metabolism, but also built in an autophagy-based ROS-induced protective mechanism to guard against oxidative stress associated with OXPHOS function during quiescence.
    WorkplaceInstitute of Biotechnology
    ContactMonika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700
    Year of Publishing2023
    Electronic addresshttps://www.tandfonline.com/doi/full/10.1080/15548627.2022.2038898
Number of the records: 1  

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