Evidence map›Paper›PMID 25499735›Full record

ReviewTrends in cell biology2015

Protecting the mitochondrial powerhouse.

Morten Scheibye-Knudsen, Evandro F Fang, Deborah L Croteau, David M Wilson, Vilhelm A Bohr

Abstract readReview
In one paragraph

Review in Trends in cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed
–field-weighted citation impact
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

187 citing papers in PubMed.

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  14. Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025
    Review
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  16. Article
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127 more citing papers are in PubMed but not listed here.

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

5 authors.

Morten Scheibye-KnudsenLaboratory of Molecular Gerontology, National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, MD 21224, USA.
Evandro F FangLaboratory of Molecular Gerontology, National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, MD 21224, USA.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, MD 21224, USA.
David M WilsonLaboratory of Molecular Gerontology, National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, MD 21224, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: vbohr@nih.gov.

Funding

DNA repair dysfunction in neurodegeneration and Alzheimer's DiseaseZIAAG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$9.5M
Mitochondrial DNA Repair Processes In Oxidative Stress And AgingZIAAG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.2M
The role of the Cockayne syndrome proteinZIAAG000722 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2023
$9.1M
Oxidative DNA Damage And Its ProcessingZIAAG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$8.4M
Oxidative DNA Damage Repair in Premature Aging and NeurodegenerationZIAAG000751 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2009 to 2019
$5.3M
OXIDATIVE STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
Intramural NIH HHS Z01 AG000733
6 · The paper itself

Abstract

Mitochondria are the oxygen-consuming power plants of cells. They provide a critical milieu for the synthesis of many essential molecules and allow for highly efficient energy production through oxidative phosphorylation. The use of oxygen is, however, a double-edged sword that on the one hand supplies ATP for cellular survival, and on the other leads to the formation of damaging reactive oxygen species (ROS). Different quality control pathways maintain mitochondria function including mitochondrial DNA (mtDNA) replication and repair, fusion-fission dynamics, free radical scavenging, and mitophagy. Further, failure of these pathways may lead to human disease. We review these pathways and propose a strategy towards a treatment for these often untreatable disorders.

Indexed as

AnimalsDNA, MitochondrialDNA RepairDNA ReplicationHomeostasisHumansMitochondriaMitophagyOxidative StressReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen SpeciesdiseaseDNA repairmitochondriamitophagyreactive oxygen species

Identifiers

PMID25499735
PMCPMC5576887

What OpenQuestion holds

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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.