Evidence map›Paper›PMID 23886445›Full record

ReviewAntioxidants & redox signaling2014

Regulation of MnSOD enzymatic activity by Sirt3 connects the mitochondrial acetylome signaling networks to aging and carcinogenesis.

Randa Tao, Athanassios Vassilopoulos, Loukia Parisiadou, Yufan Yan, David Gius

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
5.6field-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

124 citing papers in PubMed, 193 citations in OpenAlex.

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  15. Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025
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64 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

5 authors at 2 institutions in 1 country.

Randa Tao1 Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center , Houston, Texas.
Athanassios Vassilopoulos
Loukia Parisiadou
Yufan Yan
David Gius
Northwestern University · USThe University of Texas MD Anderson Cancer Center · US

Funding

Loss of mtSIRT3, Decreased MnSOD Activity, and IR Induced Genomic InstabilityR01CA152601 · NCI · VANDERBILT UNIVERSITY · PI BONINI, MARCELO G. · 2010 to 2019
$3.5M
ROS and HIFa as molecular targets for chemoprevention in Sirt3 -/- breast cancersR01CA168292 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GIUS, DAVID · 2012 to 2016
$1.9M
SIRT3 is a Mitochondrial Tumor Suppressor in ER/PR Positive Mammary TumorsR01CA152799 · NCI · VANDERBILT UNIVERSITY · PI GIUS, DAVID · 2011 to 2015
$1.6M
NCI NIH HHS 1R01CA152601-01NCI NIH HHS 1R01CA152799-01A1NCI NIH HHS 1R01CA16383801A1NCI NIH HHS 1R01CA168292-01A1NCI NIH HHS R01 CA152799NCI NIH HHS R01 CA168292
6 · The paper itself

Abstract

significanceIt is a well-established scientific observation that mammalian cells contain fidelity or watchdog proteins that maintain the correct function of cellular organelles. RECENT ADVANCES: Over the past several years, the Sirtuin deacetylase family protein Sirt3 has emerged as a mitochondrial fidelity protein that directs energy generation and regulates reactive oxygen species (ROS) scavenging proteins. Loss of function or genetic mutation of these fidelity proteins has been shown to create a cellular environment that is permissive for the development of cellular damage associated with processes such as aging and carcinogenesis. CRITICAL ISSUES: Mitochondria are the primary organelles that direct oxidative metabolism for the production of ATP; however, this is also a significant source of ROS. Thus, it is reasonable to propose that mitochondria should contain proteins that would signal downstream target molecules and/or ROS scavenger enzymes to maintain mitochondrial and cellular homeostatic poise. It is also reasonable to hypothesize that the mitochondria contain fidelity proteins similar to those found in the nucleus and cytoplasm. We discuss a new role of Sirt3 in the direction of the primary superoxide scavenger protein, manganese superoxide dismutase (MnSOD), and how the acetylation or deacetylation of several specific lysines appears to direct MnSOD enzymatic dismutase activity. FUTURE DIRECTIONS: Aberrant downstream regulation of MnSOD by Sirt3 may be a potential source of cellular damage that accumulates with aging to create a tumor-permissive phenotype. Future studies can explore the role of MnSOD in age-related illness using this new mechanism of enzymatic regulation.

Indexed as

AgingAcetylationAmino Acid SequenceAnimalsCarcinogenesisConserved SequenceGene ExpressionGene Expression RegulationHumansOxidative StressProtein Processing, Post-TranslationalSignal TransductionSirtuin 3Superoxide DismutaseSuperoxide Dismutase 2SIRT3 protein, humanSirtuin 3Superoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID23886445
PMCPMC3942696
OpenAlexW2328451459

What OpenQuestion holds

Textmetadata
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.