Evidence map›Paper›PMID 21355846›Full record

ReviewAnti-cancer agents in medicinal chemistry2011

Mitochondrial superoxide dismutase--signals of distinction.

Sumitra Miriyala, Aaron K Holley, Daret K St Clair

Abstract readReview
In one paragraph

Review in Anti-cancer agents in medicinal chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. PMHeliyon · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Insights into the Dichotomous Regulation of SOD2 in Cancer.Antioxidants (Basel, Switzerland) · 2017
    Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Sumitra MiriyalaGraduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA.
Aaron K Holley
Daret K St Clair
The Graduate Center, CUNY · US

Funding

TROPIC, CHOLINERGIC AND PATHOLOGIC CHANGES IN ALZHEIMER'S DISEASEP01AG005119 · NIA · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 1985 to 2012
$15.4M
REDOX REGULATION OF TUMOR SUPPRESSION BY MNSODR01CA073599 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 1998 to 2012
$4.0M
TRAINING GRANT IN MOLECULAR MECHANISMS OF TOXICITY.T32ES007266 · NIEHS · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI, MELLON, ISABEL W · 1990 to 2020
$3.7M
Mechansins of MnSOD expression in normal and tumor cellsR01CA049797 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 1996 to 2014
$3.3M
Rel B mediated-redox regulation of radiation therapyR01CA143428 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K, ST CLAIR, WILLIAM H · 2011 to 2015
$1.9M
MbSOD in chemotherapeutic-Induced Cardiac InjuryR01CA139843 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, DARET K · 2008 to 2012
$1.3M
Redox Modulation of Prostate CancerR01CA115801 · NCI · UNIVERSITY OF KENTUCKY · PI ST CLAIR, WILLIAM H · 2007 to 2011
$1.3M
MECHANISM OF MNSOD EXPRESSION IN NORMAL &TUMOR CELLSR29CA049797 · NCI · WAKE FOREST UNIVERSITY · PI ST CLAIR, DARET K · 1990 to 1994
–
NCI NIH HHS CA049797NCI NIH HHS CA115801NCI NIH HHS CA139843NCI NIH HHS CA143428NCI NIH HHS R01 CA049797NCI NIH HHS R01 CA073599NCI NIH HHS R01 CA115801NCI NIH HHS R01 CA139843NCI NIH HHS R01 CA143428NIA NIH HHS AG005119NIA NIH HHS P01 AG005119NIEHS NIH HHS T32 ES007266NIEHS NIH HHS T32ES007266
6 · The paper itself

Abstract

Mitochondrial superoxide dismutase (MnSOD) neutralizes the highly reactive superoxide radical (O(2)(˙-)), the first member in a plethora of mitochondrial reactive oxygen species (ROS). Over the past decades, research has extended the prevailing view of mitochondrion well beyond the generation of cellular energy to include its importance in cell survival and cell death. In the normal state of a cell, endogenous antioxidant enzyme systems maintain the level of reactive oxygen species generated by the mitochondrial respiratory chain. Mammalian mitochondria are important to the production of reactive oxygen species, which underlie oxidative damage in many pathological conditions and contribute to retrograde redox signaling from the organelle to the cytosol and nucleus. Mitochondria are further implicated in various metabolic and aging-related diseases that are now postulated to be caused by misregulation of physiological systems rather than pure accumulation of oxidative damage. Thus, the signaling mechanisms within mitochondria, and between the organelle and its environment, have gained interest as potential drug targets. Here, we discuss redox events in mitochondria that lead to retrograde signaling, the role of redox events in disease, and their potential to serve as therapeutic targets.

Indexed as

Signal TransductionHumansMitochondriaOxidation-ReductionReactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase 2Reactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID21355846
PMCPMC3427752
OpenAlexW1975671272

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.