Evidence map›Paper›PMID 32071292›Full record

ArticleCell death & disease2020

Sestrin2 protects dendritic cells against endoplasmic reticulum stress-related apoptosis induced by high mobility group box-1 protein.

Li-Xue Wang, Xiao-Mei Zhu, Yi-Nan Luo, Yao Wu, Ning Dong, Ya-Lin Tong, Yong-Ming Yao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. mTOR pathway mediates the endoplasmic reticulum stress -apoptosis of CD4+ T cell through inhibiting autophagy flux in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  19. Sestrin2 in cancer: a foe or a friend?Biomarker research · 2022
    Review
  20. The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022
    Review
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

7 authors at 2 institutions in 1 country.

Li-Xue Wang *Trauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100048, PR China.
Xiao-Mei Zhu *Trauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100048, PR China.
Yi-Nan LuoTrauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100048, PR China.
Yao WuTrauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100048, PR China.
Ning DongTrauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100048, PR China.
Ya-Lin TongDepartment of Burns and Plastic Surgery, 924th Hospital of Chinese PLA, Guilin, 541002, PR China.
Yong-Ming YaoTrauma Research Center, Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100048, PR China. c_ff@sina.com.
Chinese PLA General Hospital · CN81th Hospital of PLA · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sestrin2 (SESN2) is a highly evolutionary conserved protein and involved in different cellular responses to various stresses. However, the potential function of SESN2 in immune system remains unclear. The present study was designed to test whether dendritic cells (DCs) could express SESN2, and investigate the underlying molecular mechanism as well as its potential significance. Herein, we firstly reported that SESN2 was expressed in DCs after high mobility group box-1 protein (HMGB1) stimulation and the apoptosis of DCs was obviously increased when SESN2 gene silenced by siRNA. Cells undergone SESN2-knockdown promoted endoplasmic reticulum (ER) stress (ERS)-related cell death, markedly exacerbated ER disruption as well as the formation of dilated and aggregated structures, and they significantly aggravated the extent of ERS response. Conversely, overexpressing SESN2 DCs markedly decreased apoptotic rates and attenuated HMGB1-induced ER morphology fragment together with inhibition of ERS-related protein translation. Furthermore, sesn2

Indexed as

AnimalsApoptosisCell LineDendritic CellsDisease Models, AnimaleIF-2 KinaseEndoplasmic Reticulum StressHMGB1 ProteinMaleMice, Inbred C57BLMice, KnockoutPeroxidasesSepsisSestrinsSignal TransductionTranscription Factor CHOPDdit3 protein, mouseeIF-2 KinaseHMGB1 ProteinPeroxidasesSesn2 protein, mouseSestrinsTranscription Factor CHOP

Identifiers

PMID32071292
PMCPMC7028717
OpenAlexW3008812352

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.