Evidence map›Paper›PMID 35258392›Full record

ArticleAutophagy2022

Mitochondrial respiration supports autophagy to provide stress resistance during quiescence.

Silvia Magalhaes-Novais, Jan Blecha, Ravindra Naraine, Jana Mikesova, Pavel Abaffy, Alena Pecinova, Mirko Milosevic, Romana Bohuslavova, Jan Prochazka, Shawez Khan and 15 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023
    Pooled it
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  3. The CaInternational journal of molecular sciences · 2026
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  19. The preprogrammed anti-inflammatory phenotypes of CD11cJournal of translational medicine · 2023
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

25 authors at 7 institutions in 5 countries.

Silvia Magalhaes-NovaisInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Jan BlechaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Ravindra NaraineInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Jana MikesovaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Pavel AbaffyInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Alena PecinovaInstitute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Mirko MilosevicInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Romana BohuslavovaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Jan ProchazkaInstitute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.
Shawez KhanVIB-KU Leuven Center for Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium.
Eliska NovotnaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Radek SindelkaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.
Radek MachanFaculty of Science, Charles University, Prague, Czech Republic.
Mieke DewerchinVIB-KU Leuven Center for Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium.
Erik VlcakInstitute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.
Joanna KaluckaDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID 0000-0003-4887-7672
Sona Stemberkova HubackovaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.ORCID 0000-0002-3454-6840
Ales BendaFaculty of Science, Charles University, Prague, Czech Republic.
Jermaine GoveiaVIB-KU Leuven Center for Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium.
Tomas MracekInstitute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.ORCID 0000-0002-9492-0718
Cyril BarinkaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.ORCID 0000-0003-2751-3060
Peter CarmelietVIB-KU Leuven Center for Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium.
Jiri NeuzilInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.ORCID 0000-0002-2478-2460
Katerina RohlenovaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.ORCID 0000-0003-3964-8472
Jakub RohlenaInstitute of Biotechnology, Czech Academy of Sciences, BIOCEV, Vestec, Czech Republic.ORCID 0000-0001-5427-6502
Czech Academy of Sciences, Institute of Biotechnology · CZCharles University · CZCzech Academy of Sciences · CZVIB-KU Leuven Center for Cancer Biology · BEAarhus University · DKGriffith University · AUSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AutophagyInflammatory Bowel DiseasesAdenosine TriphosphateAMP-Activated Protein KinasesAnimalsCysteineDextransDNA, MitochondrialEndothelial CellsFibroblastsFormaldehydeHumansIsothiocyanatesLipopolysaccharidesMechanistic Target of Rapamycin Complex 1MiceAdenosine TriphosphateAMP-Activated Protein KinasesCysteineDextransDNA, MitochondrialFormaldehydeIsothiocyanatesLipopolysaccharidesMechanistic Target of Rapamycin Complex 1Microtubule-Associated Proteinsphenethyl isothiocyanatePhosphatidylethanolaminesReactive Oxygen SpeciesSirolimusATG4Bbiosynthesiscell deathelectron transport chainendothelial cellsmitochondriaoxidative phosphorylationoxidative stressreactive oxygen species

Identifiers

PMID35258392
PMCPMC9542673
OpenAlexW4220758320

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.