Evidence map›Paper›PMID 33820957›Full record

ArticleScientific reports2021

Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock.

Peng Wang, Li-Na Jiang, Chen Wang, Ying Li, Meng Yin, Hui-Bo Du, Hong Zhang, Ze-Hua Fan, Yan-Xu Liu, Meng Zhao and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. 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

15 authors at 2 institutions in 1 country.

Peng WangInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Li-Na JiangInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Chen WangInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Ying LiInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Meng YinInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Hui-Bo DuInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Hong ZhangInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Ze-Hua FanInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Yan-Xu LiuInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Meng ZhaoInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
An-Ling KangInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Ding-Ya FengInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Shu-Guang LiInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China.
Chun-Yu NiuBasic Medical College, Hebei Medical University, Zhongshan East Road 361, Shijiazhuang, Hebei, 075000, People's Republic of China. ncylxf@126.com.
Zi-Gang ZhaoInstitute of Microcirculation, Hebei North University, Diamond South Road 11, Zhangjiakou, Hebei, 075000, People's Republic of China. zzghyl@126.com.
Hebei North University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim is to investigate that 17β-estradiol (E2)/estrogen receptors (ERs) activation normalizes splenic CD4 + T lymphocytes proliferation and cytokine production through inhibition of endoplasmic reticulum stress (ERS) following hemorrhage. The results showed that hemorrhagic shock (hemorrhage through femoral artery, 38-42 mmHg for 90 min followed by resuscitation of 30 min and subsequent observation period of 180 min) decreased the CD4

Indexed as

Activating Transcription Factor 6AnimalsBiomarkersCD4-Positive T-LymphocytesCell ProliferationCytokinesEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEstradiolHeat-Shock ProteinsMaleModels, BiologicalRatsRats, WistarShock, HemorrhagicSpleenActivating Transcription Factor 6Atf6 protein, ratBiomarkersCytokinesEndoplasmic Reticulum Chaperone BiPEstradiolGRP78 protein, ratHeat-Shock Proteins

Identifiers

PMID33820957
PMCPMC8021564
OpenAlexW3143840319

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.