Evidence map›Paper›PMID 19398959›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2009

Transgenic mitochondrial superoxide dismutase and mitochondrially targeted catalase prevent antiretroviral-induced oxidative stress and cardiomyopathy.

James J Kohler, Ioan Cucoranu, Earl Fields, Elgin Green, Stanley He, Amy Hoying, Rodney Russ, Allison Abuin, David Johnson, Seyed H Hosseini and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-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

30 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Diabetes, metabolic syndrome and obesity : targets and therapy · 2018
    Article
  5. Article
  6. Astragalus polysaccharides improve cardiomyopathy in STZ-induced diabetic mice and heterozygous (SOD2+/-) knockout mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  7. Drug-induced mitochondrial dysfunction and cardiotoxicity.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Aging and HIV/AIDS: pathogenetic role of therapeutic side effects.Laboratory investigation; a journal of technical methods and pathology · 2014
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Mouse Models of Oxidative Stress Indicate a Role for Modulating Healthy Aging.Journal of clinical & experimental pathology · 2012
    Article
  19. The role of transporters in the toxicity of nucleoside and nucleotide analogs.Expert opinion on drug metabolism & toxicology · 2012
    Review
  20. Drug-induced oxidative stress and toxicity.Journal of toxicology · 2012
    Article
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

12 authors at 1 institution in 1 country.

James J KohlerDepartment of Pathology, Emory University, Atlanta, GA, USA.
Ioan Cucoranu
Earl Fields
Elgin Green
Stanley He
Amy Hoying
Rodney Russ
Allison Abuin
David Johnson
Seyed H Hosseini
C Michael Raper
William Lewis
Emory University · US

Funding

CARDIOMYOPATHY IN AIDSR01HL059798 · NHLBI · UNIVERSITY OF CINCINNATI · PI LEWIS, WILLIAM · 1997 to 2009
$2.8M
Cardiomyocyte Cell Cycle, Antiretrovirals and AIDSR01HL079867 · NHLBI · EMORY UNIVERSITY · PI LEWIS, WILLIAM · 2006 to 2010
$1.9M
NHLBI NIH HHS R01 HL059798NHLBI NIH HHS R01 HL079867
6 · The paper itself

Abstract

Transgenic mice (TG) were used to define mitochondrial oxidative stress and cardiomyopathy (CM) induced by zidovudine (AZT), an antiretroviral used to treat HIV/AIDS. Genetically engineered mice either depleted or overexpressed mitochondrial superoxide dismutase (SOD2(+/-) KOs and SOD2-OX, respectively) or expressed mitochondrially targeted catalase (mCAT). TGs and wild-type (WT) littermates were treated (oral AZT, 35 days). Cardiac mitochondrial H(2)O(2), aconitase activity, histology and ultrastructure were analyzed. Left ventricle (LV) mass and LV end-diastolic dimension were determined echocardiographically. AZT induced cardiac oxidative stress and LV dysfunction in WTs. Cardiac mitochondrial H(2)O(2) increased and aconitase was inactivated in SOD2(+/-) KOs, and cardiac dysfunction was worsened by AZT. Conversely, the cardiac function in SOD2-OX and mCAT hearts was protected. In SOD2-OX and mCAT TG hearts, mitochondrial H(2)O(2), LV mass and LV cavity volume resembled corresponding values from vehicle-treated WTs. AZT worsens cardiac dysfunction and increases mitochondrial H(2)O(2) in SOD2(+/-) KO. Conversely, both SOD2-OX and mCAT TGs prevent or attenuate AZT-induced cardiac oxidative stress and LV dysfunction. As dysfunctional changes are ameliorated by decreasing and worsened by increasing H(2)O(2) abundance, oxidative stress from H(2)O(2) is crucial pathogenetically in AZT-induced mitochondrial CM.

Indexed as

Aconitate HydrataseAnimalsAnti-HIV AgentsCardiomyopathiesCatalaseFemaleGene ExpressionHydrogen PeroxideMaleMiceMice, CongenicMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, Electron, TransmissionMitochondria, HeartAconitate HydrataseAnti-HIV AgentsCatalaseHydrogen PeroxideSuperoxide DismutaseSuperoxide Dismutase 2Zidovudine

Identifiers

PMID19398959
PMCPMC7712498
OpenAlexW2039582261

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.