Evidence map›Paper›PMID 25276767›Full record

ReviewBioMed research international2014

Superoxide dismutase 1 loss disturbs intracellular redox signaling, resulting in global age-related pathological changes.

Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Hidetoshi Nojiri, Naotaka Izuo, Koutaro Yokote, Takahiko Shimizu

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. 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
3.3field-weighted citation impact, top 8% 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, 59 citations in OpenAlex.

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  13. Regulation of immune cell function by nicotinamide nucleotide transhydrogenase.American journal of physiology. Cell physiology · 2022
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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

7 authors at 2 institutions in 1 country.

Kenji WatanabeDepartment of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan ; Department of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0003-1707-1676
Shuichi ShibuyaDepartment of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0003-4050-0934
Yusuke OzawaDepartment of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0002-4660-6193
Hidetoshi NojiriDepartment of Orthopaedics, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-0033, Japan.ORCID 0000-0002-2359-3393
Naotaka IzuoDepartment of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0002-2642-5045
Koutaro YokoteDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0003-3033-4813
Takahiko ShimizuDepartment of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.ORCID 0000-0002-3351-3342
Chiba University · JPJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1(-/-)) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1(-/-) mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1(-/-) mice.

Indexed as

Signal TransductionAgingAnimalsAntioxidantsHumansIntracellular SpaceOxidation-ReductionSuperoxide DismutaseSuperoxide Dismutase-1AntioxidantsSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID25276767
PMCPMC4170698
OpenAlexW2160523206

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.