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Mitochondrial respiration supports autophagy to provide stress resistance during quiescence

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F22%3A00557875" target="_blank" >RIV/68378050:_____/22:00557875 - isvavai.cz</a>

  • Alternative codes found

    RIV/86652036:_____/22:00557875 RIV/67985823:_____/22:00557875 RIV/00023001:_____/22:00083463 RIV/00216208:11310/22:10456185

  • Result on the web

    <a href="https://www.tandfonline.com/doi/full/10.1080/15548627.2022.2038898" target="_blank" >https://www.tandfonline.com/doi/full/10.1080/15548627.2022.2038898</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1080/15548627.2022.2038898" target="_blank" >10.1080/15548627.2022.2038898</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Mitochondrial respiration supports autophagy to provide stress resistance during quiescence

  • Original language description

    Mitochondrial 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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10601 - Cell biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2022

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Autophagy

  • ISSN

    1554-8627

  • e-ISSN

    1554-8635

  • Volume of the periodical

    18

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    19

  • Pages from-to

    2409-2426

  • UT code for WoS article

    000766134900001

  • EID of the result in the Scopus database

    2-s2.0-85126384039