Evidence map›Paper›PMID 37011700›Full record

ArticleFree radical biology & medicine2023

Mitochondrial OGG1 expression reduces age-associated neuroinflammation by regulating cytosolic mitochondrial DNA.

Mansoor Hussain, Xixia Chu, Burcin Duan Sahbaz, Samuel Gray, Komal Pekhale, Jae-Hyeon Park, Deborah L Croteau, Vilhelm A Bohr

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

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  13. [HeZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
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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

8 authors at 2 institutions in 2 countries.

Mansoor HussainDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA.
Xixia ChuDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA.
Burcin Duan SahbazDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA.
Samuel GrayDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA.
Komal PekhaleDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA.
Jae-Hyeon ParkDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA.
Deborah L CroteauDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA; Computational Biology & Genomics Core, National Institute on Aging, Baltimore, MD, 21224, USA.
Vilhelm A BohrDNA repair section, National Institute on Aging, Baltimore, MD, 21224, USA; Danish Center for Healthy Aging, University of Copenhagen, Copenhagen, 2200, Denmark. Electronic address: vbohr@sund.ku.dk.
National Institute on Aging · USUniversity of Copenhagen · DK

Funding

Linking Defects in DNA Repair to Mitochondrial Dysfunction in Alzheimer's DiseaseZIAAG000578 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2019 to 2023
$2.6M
REPAIR OF OXIDATIVE DNA DAMAGEZ01AG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1994 to 2008
$1.3M
GROWTH ARREST AND DNA DAMAGE INDUCIBLE GENE GADD153--REGULATION BY DNA DAMAGEZ01AG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM · 1992 to 2008
$310k
Intramural NIH HHS Z01 AG000723Intramural NIH HHS Z01 AG000727
6 · The paper itself

Abstract

Aging is accompanied by a decline in DNA repair efficiency, which leads to the accumulation of different types of DNA damage. Age-associated chronic inflammation and generation of reactive oxygen species exacerbate the aging process and age-related chronic disorders. These inflammatory processes establish conditions that favor accumulation of DNA base damage, especially 8-oxo-7,8 di-hydroguanine (8-oxoG), which in turn contributes to various age associated diseases. 8-oxoG is repaired by 8-oxoG glycosylase1 (OGG1) through the base excision repair (BER) pathway. OGG1 is present in both the cell nucleus and in mitochondria. Mitochondrial OGG1 has been implicated in mitochondrial DNA repair and increased mitochondrial function. Using transgenic mouse models and cell lines that have been engineered to have enhanced expression of mitochondria-targeted OGG1 (mtOGG1), we show that elevated levels of mtOGG1 in mitochondria can reverse aging-associated inflammation and improve functions. Old male mtOGG1

Indexed as

DNA GlycosylasesDNA, MitochondrialAnimalsDNA DamageDNA RepairFemaleHumansInflammationMaleMiceMice, TransgenicMitochondriaNeuroinflammatory DiseasesOxidative StressDNA GlycosylasesDNA, MitochondrialOgg1 protein, mouseoxoguanine glycosylase 1, humanAgingBase excision repairDNA repairMitochondriamtOGG1Ogg1

Identifiers

PMID37011700
PMCPMC10247526
OpenAlexW4362453915

What OpenQuestion holds

Textmetadata
LicenceTDM
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.