Evidence map›Paper›PMID 25036887›Full record

ReviewBiomolecules2014

New perspectives on oxidized genome damage and repair inhibition by pro-oxidant metals in neurological diseases.

Joy Mitra, Erika N Guerrero, Pavana M Hegde, Haibo Wang, Istvan Boldogh, Kosagi Sharaf Rao, Sankar Mitra, Muralidhar L Hegde

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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  9. Synthesis and anti-myocarditis activity in a multifunctional lanthanide microporous metal-organic framework with 1D helical chain building units.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
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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 3 institutions in 3 countries.

Joy MitraDepartment of Radiation Oncology, Houston Methodist Research Institute, Affiliate of Weill Medical College of Cornell University, 6550 Fannin St, Smith 8-030, Houston, TX 77030, USA. jmitra@houstonmethodist.org.
Erika N GuerreroDepartment of Radiation Oncology, Houston Methodist Research Institute, Affiliate of Weill Medical College of Cornell University, 6550 Fannin St, Smith 8-030, Houston, TX 77030, USA. kjr5n2009@gmail.com.
Pavana M HegdeDepartment of Radiation Oncology, Houston Methodist Research Institute, Affiliate of Weill Medical College of Cornell University, 6550 Fannin St, Smith 8-030, Houston, TX 77030, USA. pdixit@HoustonMethodist.org.
Haibo WangDepartment of Radiation Oncology, Houston Methodist Research Institute, Affiliate of Weill Medical College of Cornell University, 6550 Fannin St, Smith 8-030, Houston, TX 77030, USA. hwang@houstonmethodist.org.
Istvan BoldoghDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA. sboldogh@utmb.edu.
Kosagi Sharaf RaoCentre for Neuroscience, Institute for Scientific Research and Technology Services (INDICASAT-AIP), City of Knowledge, P.O. Box 0843-01103, Panama. kjr5n2009@gmail.com.
Sankar MitraDepartment of Radiation Oncology, Houston Methodist Research Institute, Affiliate of Weill Medical College of Cornell University, 6550 Fannin St, Smith 8-030, Houston, TX 77030, USA. smitra2@houstonmethodist.org.
Muralidhar L HegdeDepartment of Radiation Oncology, Houston Methodist Research Institute, Affiliate of Weill Medical College of Cornell University, 6550 Fannin St, Smith 8-030, Houston, TX 77030, USA. mlhegde@houstonmethodist.org.
Houston Methodist · USInstituto de Investigaciones Científicas y Servicios de Alta Tecnología · PAThe University of Texas Medical Branch at Galveston · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
Virus, Tissue Culture and ImmunoassayP01AI062885 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CASOLA, ANTONELLA · 2005 to 2022
$23.9M
"Repair Co-ordination of Radiation-Induced Clustered Damage In Mammalian Genomes"R01CA158910 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MITRA, SANKAR · 2012 to 2016
$1.6M
Linkage of Lung Inflammation to 8-oxoguanine and OGG1R01ES018948 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BOLDOGH, ISTVAN STEVEN · 2010 to 2014
$1.5M
NCI NIH HHS P01 CA092584NCI NIH HHS R01 CA158910NIAID NIH HHS P01 AI062885NIEHS NIH HHS R01 ES018948
6 · The paper itself

Abstract

The primary cause(s) of neuronal death in most cases of neurodegenerative diseases, including Alzheimer's and Parkinson's disease, are still unknown. However, the association of certain etiological factors, e.g., oxidative stress, protein misfolding/aggregation, redox metal accumulation and various types of damage to the genome, to pathological changes in the affected brain region(s) have been consistently observed. While redox metal toxicity received major attention in the last decade, its potential as a therapeutic target is still at a cross-roads, mostly because of the lack of mechanistic understanding of metal dyshomeostasis in affected neurons. Furthermore, previous studies have established the role of metals in causing genome damage, both directly and via the generation of reactive oxygen species (ROS), but little was known about their impact on genome repair. Our recent studies demonstrated that excess levels of iron and copper observed in neurodegenerative disease-affected brain neurons could not only induce genome damage in neurons, but also affect their repair by oxidatively inhibiting NEIL DNA glycosylases, which initiate the repair of oxidized DNA bases. The inhibitory effect was reversed by a combination of metal chelators and reducing agents, which underscore the need for elucidating the molecular basis for the neuronal toxicity of metals in order to develop effective therapeutic approaches. In this review, we have focused on the oxidative genome damage repair pathway as a potential target for reducing pro-oxidant metal toxicity in neurological diseases.

Indexed as

DNA DamageDNA RepairAnimalsGenomeHumansMetalsNeurodegenerative DiseasesOxidation-ReductionReactive Oxygen SpeciesMetalsReactive Oxygen Species

Identifiers

PMID25036887
PMCPMC4192668
OpenAlexW2028551252

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.