Evidence map›Paper›PMID 21930250›Full record

ReviewMitochondrion2012

Cytoprotection by the modulation of mitochondrial electron transport chain: the emerging role of mitochondrial STAT3.

Karol Szczepanek, Qun Chen, Andrew C Larner, Edward J Lesnefsky

Abstract readReview
In one paragraph

Review in Mitochondrion, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
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  7. OGT controls mammalian cell viability by regulating the proteasome/mTOR/ mitochondrial axis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022
    Review
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16 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Karol SzczepanekDepartment of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Qun Chen
Andrew C Larner
Edward J Lesnefsky
Virginia Commonwealth University · USHunter Holmes McGuire VA Medical Center · US

Funding

SULFHYDRYL STATUS IN THE AGING HEART: ROLE OF GLUTAREDOXINP01AG015885 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI LESNEFSKY, EDWARD J · 1998 to 2008
$8.1M
Pathways that Regulate Antigrowth Effects of InterferonsR01CA098924 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LARNER, ANDREW CHARLES · 2004 to 2008
$1.4M
The Jak/Stat Pathway and Mitochondrial FunctionR01GM101677 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI LARNER, ANDREW CHARLES · 2012 to 2015
$1.1M
NCI NIH HHS CA098924NCI NIH HHS R01 CA098924NIA NIH HHS 2P01AG15885NIA NIH HHS P01 AG015885NIGMS NIH HHS R01 GM101677
6 · The paper itself

Abstract

The down regulation of mitochondrial electron transport is an emerging mechanism of cytoprotective intervention that is effective in pathologic settings such as myocardial ischemia and reperfusion when the continuation of mitochondrial respiration produces reactive oxygen species, mitochondrial calcium overload, and the release of cytochrome c to activate cell death programs. The initial target of deranged electron transport is the mitochondria themselves. In the first part of this review, we describe this concept and summarize different approaches used to regulate mitochondrial respiration by targeting complex I as a proximal site in the electron transport chain (ETC) in order to favor the cytoprotection. The second part of the review highlights the emerging role of signal transducer and activator of transcription 3 (STAT3) in the direct, non-transcriptional regulation of ETC, as an example of a genetic approach to modulate respiration. Recent studies indicate that a pool of STAT3 resides in the mitochondria where it is necessary for the maximal activity of complexes I and II of the electron transport chain (ETC). The overexpression of mitochondrial-targeted STAT3 results in a partial blockade of electron transport at complexes I and II that does not impair mitochondrial membrane potential nor enhance the production of reactive oxygen species (ROS). The targeting of transcriptionally-inactive STAT3 to mitochondria attenuates damage to mitochondria during cell stress, resulting in decreased production of ROS and retention of cytochrome c by mitochondria. The overexpression of STAT3 targeted to mitochondria unveils a novel protective approach mediated by modulation of mitochondrial respiration that is independent of STAT3 transcriptional activity. The limitation of mitochondrial respiration under pathologic circumstances can be approached by activation and overexpression of endogenous signaling mechanisms in addition to pharmacologic means. The regulation of mitochondrial respiration comprises a cardioprotective paradigm to decrease cellular injury during ischemia and reperfusion.

Indexed as

CytoprotectionAnimalsDown-RegulationElectron Transport Complex IElectron Transport Complex IIHumansMitochondrial ProteinsReactive Oxygen SpeciesSTAT3 Transcription FactorElectron Transport Complex IElectron Transport Complex IIMitochondrial ProteinsReactive Oxygen SpeciesSTAT3 Transcription Factor

Identifiers

PMID21930250
PMCPMC3278553
OpenAlexW1991845993

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.