Evidence map›Paper›PMID 24344202›Full record

ArticleMolecular and cellular biology2014

SIRT3 deacetylates and activates OPA1 to regulate mitochondrial dynamics during stress.

Sadhana A Samant, Hannah J Zhang, Zhigang Hong, Vinodkumar B Pillai, Nagalingam R Sundaresan, Donald Wolfgeher, Stephen L Archer, David C Chan, Mahesh P Gupta

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 1 pooled it
9.9field-weighted citation impact, top 1% 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

228 citing papers in PubMed, 1 synthesis or guideline pooled it, 421 citations in OpenAlex.

  1. Pooled it
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  12. Metrnl in health and disease: tissue-specific actions and signaling networks.Apoptosis : an international journal on programmed cell death · 2026
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168 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

9 authors at 3 institutions in 2 countries.

Sadhana A SamantDepartment of Surgery, University of Chicago, Chicago, Illinois, USA.
Hannah J Zhang
Zhigang Hong
Vinodkumar B Pillai
Nagalingam R Sundaresan
Donald Wolfgeher
Stephen L Archer
David C Chan
Mahesh P Gupta
University of Chicago · USHoward Hughes Medical Institute · USQueen's University · CA

Funding

O2 sensing in the human and rabbit ductus arteriosus.R01HL071115 · NHLBI · UNIVERSITY OF CHICAGO · PI ARCHER, STEPHEN L · 2004 to 2015
$3.1M
The Role of PARP-SIR2 Signaling in Heart FailureR01HL083423 · NHLBI · UNIVERSITY OF CHICAGO · PI GUPTA, MAHESH P · 2007 to 2011
$2.4M
Blocking cardiac toxicity of anticancer drugsR01HL117041 · NHLBI · UNIVERSITY OF CHICAGO · PI GUPTA, MAHESH P · 2013 to 2016
$1.8M
Activation of sirtuins to prevent adverse cardiac remodeling after CABGR01HL111455 · NHLBI · UNIVERSITY OF CHICAGO · PI GUPTA, MAHESH P · 2013 to 2016
$1.6M
The Role of DRP-1 and Mitochondrial Fission in Pulmonary Arterial HypertensionR01HL113003 · NHLBI · QUEEN'S UNIVERSITY AT KINGSTON · PI ARCHER, STEPHEN L · 2013 to 2016
$1.1M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL071115NHLBI NIH HHS R01 HL083423NHLBI NIH HHS R01 HL111455NHLBI NIH HHS R01 HL113003NHLBI NIH HHS R01 HL117041NHLBI NIH HHS R01 HL83423
6 · The paper itself

Abstract

Mitochondrial morphology is regulated by the balance between two counteracting mitochondrial processes of fusion and fission. There is significant evidence suggesting a stringent association between morphology and bioenergetics of mitochondria. Morphological alterations in mitochondria are linked to several pathological disorders, including cardiovascular diseases. The consequences of stress-induced acetylation of mitochondrial proteins on the organelle morphology remain largely unexplored. Here we report that OPA1, a mitochondrial fusion protein, was hyperacetylated in hearts under pathological stress and this posttranslational modification reduced the GTPase activity of the protein. The mitochondrial deacetylase SIRT3 was capable of deacetylating OPA1 and elevating its GTPase activity. Mass spectrometry and mutagenesis analyses indicated that in SIRT3-deficient cells OPA1 was acetylated at lysine 926 and 931 residues. Overexpression of a deacetylation-mimetic version of OPA1 recovered the mitochondrial functions of OPA1-null cells, thus demonstrating the functional significance of K926/931 acetylation in regulating OPA1 activity. Moreover, SIRT3-dependent activation of OPA1 contributed to the preservation of mitochondrial networking and protection of cardiomyocytes from doxorubicin-mediated cell death. In summary, these data indicated that SIRT3 promotes mitochondrial function not only by regulating activity of metabolic enzymes, as previously reported, but also by regulating mitochondrial dynamics by targeting OPA1.

Indexed as

AcetylationAnimalsCell DeathCell Line, TumorCells, CulturedFibroblastsGTP PhosphohydrolasesHeartHeLa CellsHumansMiceMice, TransgenicMitochondriaMitochondrial DynamicsMitochondrial ProteinsMyocytes, CardiacGTP PhosphohydrolasesMitochondrial ProteinsOpa1 protein, mouseSirt3 protein, mouseSirtuin 3

Identifiers

PMID24344202
PMCPMC4023816
OpenAlexW2163051782

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.