Evidence map›Paper›PMID 32059483›Full record

ArticleCells2020

SIRT1 Protects the Heart from ER Stress-Induced Injury by Promoting eEF2K/eEF2-Dependent Autophagy.

Julie Pires Da Silva, Kevin Monceaux, Arnaud Guilbert, Mélanie Gressette, Jérôme Piquereau, Marta Novotova, Renée Ventura-Clapier, Anne Garnier, Christophe Lemaire

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 62 citations in OpenAlex.

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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 2 institutions in 2 countries.

Julie Pires Da SilvaUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Kevin MonceauxUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Arnaud GuilbertUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Mélanie GressetteUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Jérôme PiquereauUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Marta NovotovaInstitute of Experimental Endocrinology, Biomedical Centre SAS, 833 06 Bratislava, Slovakia.
Renée Ventura-ClapierUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Anne GarnierUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Christophe LemaireUniversité Paris-Saclay, Inserm, UMR-S 1180, 92296 Châtenay-Malabry, France.
Inserm · FRInstitute of Experimental Endocrinology of the Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many recent studies have demonstrated the involvement of endoplasmic reticulum (ER) stress in the development of cardiac diseases and have suggested that modulation of ER stress response could be cardioprotective. Previously, we demonstrated that the deacetylase Sirtuin 1 (SIRT1) attenuates ER stress response and promotes cardiomyocyte survival. Here, we investigated whether and how autophagy plays a role in SIRT1-afforded cardioprotection against ER stress. The results revealed that protective autophagy was initiated before cell death in response to tunicamycin (TN)-induced ER stress in cardiac cells. SIRT1 inhibition decreased ER stress-induced autophagy, whereas its activation enhanced autophagy. In response to TN- or isoproterenol-induced ER stress, mice deficient for SIRT1 exhibited suppressed autophagy along with exacerbated cardiac dysfunction. At the molecular level, we found that in response to ER stress (i) the extinction of eEF2 or its kinase eEF2K not only reduced autophagy but further activated cell death, (ii) inhibition of SIRT1 inhibited the phosphorylation of eEF2, (iii) eIF2α co-immunoprecipitated with eEF2K, and (iv) knockdown of eIF2α reduced the phosphorylation of eEF2. Our results indicate that in response to ER stress, SIRT1 activation promotes cardiomyocyte survival by enhancing autophagy at least through activation of the eEF2K/eEF2 pathway.

Indexed as

AutophagyEndoplasmic Reticulum StressAnimalsElongation Factor 2 KinaseEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsIsoproterenolMiceMice, Inbred C57BLMice, KnockoutMicrotubule-Associated ProteinsMyocytes, CardiacRatsRNA InterferenceRNA, Small InterferingSequestosome-1 ProteinAnxa3 protein, ratEef2k protein, mouseElongation Factor 2 KinaseEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsIsoproterenolMicrotubule-Associated ProteinsRNA, Small InterferingSequestosome-1 ProteinSirt1 protein, mouseSirtuin 1Sqstm1 protein, ratTunicamycinautophagy/mitophagycardioprotectioncell deathendoplasmic reticulum stressSirtuin 1

Identifiers

PMID32059483
PMCPMC7072417
OpenAlexW3005907966

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.