Evidence map›Paper›PMID 30695691›Full record

ReviewFree radical biology & medicine2019

Does Bach1 & c-Myc dependent redox dysregulation of Nrf2 & adaptive homeostasis decrease cancer risk in ageing?

Kelvin J A Davies, Henry Jay Forman

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

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  17. The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging.Oxidative medicine and cellular longevity · 2021
    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

2 authors at 1 institution in 1 country.

Kelvin J A DaviesLeonard Davis School of Gerontology of the Ethel Percy Andrus gerontology Center, University of Southern California, Los Angeles, CA, 90089-0191, USA; Division of Molecular & Computational Biology, Department of Biological Sciences of the College of Letters, Arts & Sciences, University of Southern California, Los Angeles, CA 90089-0191, USA. Electronic address: kelvin@usc.edu.
Henry Jay FormanLeonard Davis School of Gerontology of the Ethel Percy Andrus gerontology Center, University of Southern California, Los Angeles, CA, 90089-0191, USA.
University of Southern California · US

Funding

OXYGEN RADICAL TOXICITY AND RED CELL PROTEIN DEGRADATIONR01ES003598 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DAVIES, KELVIN J. A. · 1988 to 2017
$5.7M
USC Geroscience Training in the Biology of AgingT32AG052374 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Sean P CURRAN · 2016 to 2026
$5.3M
Human models of the particulate-induced inflammatory/antioxidant axis in agingR01ES023864 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FORMAN, HENRY JAY · 2015 to 2019
$2.4M
ADAPT 78 IN OXIDANT STRESS, AGING AND NEURODEGENERATIONR01AG016256 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DAVIES, KELVIN J. A. · 2000 to 2004
$1.6M
Human models of the particulate-induced inflammatory/antioxidant axis in agingR56ES023864 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FORMAN, HENRY JAY · 2014 to 2014
$150k
Oxygen Radical Toxicity and Protein DegradationR56ES003598 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DAVIES, KELVIN J. A. · 2012 to 2012
$138k
Biological Sciences Program at The Gerontological Society of America's Annual Scientific MeetingR13AG059414 · NIA · GERONTOLOGICAL SOCIETY OF AMERICA · PI D'ANTONIO, PATRICIA M, DAVIES, KELVIN J. A. · 2018 to 2018
$50k
NIA NIH HHS R01 AG016256NIA NIH HHS R13 AG059414NIA NIH HHS T32 AG052374NIEHS NIH HHS R01 ES003598NIEHS NIH HHS R01 ES023864NIEHS NIH HHS R56 ES003598NIEHS NIH HHS R56 ES023864
6 · The paper itself

Abstract

The Keap1-Nrf2 signal transduction pathway plays a major role in oxidant and electrophile induction of adaptive homeostasis that transiently and reversibly increases cellular and organismal protection from stress. By expanding (and then contracting) the normal homeostatic range of expression of stress-protective genes, Nrf2 allows us to cope with fluctuations in stress levels. Two major inhibitors of Nrf2 are Bach1 and c-Myc which normally serve the important function of turning off adaptation when appropriate. We have found, however, that both Bach1 and c-Myc levels increase substantially with age and that older human cells, worms, flies, and mice loose Nrf2-dependent signaling and adaptive homeostasis. Nrf2 has also been linked with increased risk of cancers, and cancer incidence certainly increases with age. Here we propose that the age-dependent increase in Bach1 and c-Myc may actually cause the age-dependent decline in Nrf2 signaling and adaptive homeostasis, and that this is a coordinated attempt to minimize the age-dependent increase in cancer incidence. In other words, we may trade off adaptive homeostasis for a lower risk of cancer by increasing Bach1 and c-Myc in ageing.

Indexed as

HomeostasisSignal TransductionAgingBasic-Leucine Zipper Transcription FactorsCytoprotectionHumansNeoplasmsNF-E2-Related Factor 2Oxidative StressProto-Oncogene Proteins c-mycRisk FactorsBACH1 protein, humanBasic-Leucine Zipper Transcription FactorsMYC protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2Proto-Oncogene Proteins c-mycAdaptive homeostasisAgeingAgingAntioxidant enzymesAntioxidantsBach1Cancerc-MycElectrophilesNrf2OxidantsProteasome

Identifiers

PMID30695691
PMCPMC6588462
OpenAlexW2913211229

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.