Evidence map›Paper›PMID 25050144›Full record

ArticleOxidative medicine and cellular longevity2014

Bach1 deficiency and accompanying overexpression of heme oxygenase-1 do not influence aging or tumorigenesis in mice.

Kazushige Ota, Andrey Brydun, Ari Itoh-Nakadai, Jiying Sun, Kazuhiko Igarashi

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Bach1: Function, Regulation, and Involvement in Disease.Oxidative medicine and cellular longevity · 2018
    Review
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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

5 authors at 2 institutions in 1 country.

Kazushige OtaDepartment of Biochemistry, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai 980-0872, Japan ; Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai 980-0872, Japan.
Andrey BrydunDepartment of Biochemistry, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai 980-0872, Japan.ORCID 0000-0002-6180-995X
Ari Itoh-NakadaiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai 980-0872, Japan.
Jiying SunDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8551, Japan.
Kazuhiko IgarashiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai 980-0872, Japan ; Center for Regulatory Epigenome and Diseases, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai 980-0872, Japan.ORCID 0000-0002-2470-2475
Tohoku University · JPHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress contributes to both aging and tumorigenesis. The transcription factor Bach1, a regulator of oxidative stress response, augments oxidative stress by repressing the expression of heme oxygenase-1 (HO-1) gene (Hmox1) and suppresses oxidative stress-induced cellular senescence by restricting the p53 transcriptional activity. Here we investigated the lifelong effects of Bach1 deficiency on mice. Bach1-deficient mice showed longevity similar to wild-type mice. Although HO-1 was upregulated in the cells of Bach1-deficient animals, the levels of ROS in Bach1-deficient HSCs were comparable to those in wild-type cells. Bach1(-/-); p53(-/-) mice succumbed to spontaneous cancers as frequently as p53-deficient mice. Bach1 deficiency significantly altered transcriptome in the liver of the young mice, which surprisingly became similar to that of wild-type mice during the course of aging. The transcriptome adaptation to Bach1 deficiency may reflect how oxidative stress response is tuned upon genetic and environmental perturbations. We concluded that Bach1 deficiency and accompanying overexpression of HO-1 did not influence aging or p53 deficiency-driven tumorigenesis. Our results suggest that it is useful to target Bach1 for acute injury responses without inducing any apparent deteriorative effect.

Indexed as

AgingAnimalsBasic-Leucine Zipper Transcription FactorsCarcinogenesisGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHematopoietic Stem CellsHeme Oxygenase-1LiverLongevityMice, Inbred C57BLTranscriptomeTumor Suppressor Protein p53Bach1 protein, mouseBasic-Leucine Zipper Transcription FactorsHeme Oxygenase-1Tumor Suppressor Protein p53

Identifiers

PMID25050144
PMCPMC4094857
OpenAlexW2170324708

What OpenQuestion holds

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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.