Evidence map›Paper›PMID 35514298›Full record

ArticleInternational journal of molecular medicine2022

Selective inhibition of JNK located on mitochondria protects against mitochondrial dysfunction and cell death caused by endoplasmic reticulum stress in mice with LPS‑induced ALI/ARDS.

Congcong Li, Debin Ma, Yan Chen, Wei Liu, Faguang Jin, Liyan Bo

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  8. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  9. Article
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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

6 authors at 2 institutions in 1 country.

Congcong LiDepartment of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command, Shenyang, Liaoning 110016, P.R. China.
Debin MaDepartment of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command, Shenyang, Liaoning 110016, P.R. China.
Yan ChenDepartment of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command, Shenyang, Liaoning 110016, P.R. China.
Wei LiuDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Faguang JinDepartment of Respiratory and Critical Care Medicine, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Liyan BoDepartment of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command, Shenyang, Liaoning 110016, P.R. China.
General Hospital of Shenyang Military Region · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Few pharmacological interventions are able to improve the mortality rate of acute lung injury and acute respiratory distress syndrome (ALI/ARDS). The aim of this research was to elucidate whether endoplasmic reticulum (ER) stress and c‑Jun‑N‑terminal kinase (JNK)‑mitochondria pathways serve important roles in ALI/ARDS and to determine whether the key component Sab is a potential treatment target. The current study investigated the activation of ER stress and the JNK pathway, the content of JNK located on the mitochondria during ER stress and lipopolysaccharide (LPS)‑induced ALI/ARDS by western blot analysis. The treatment effects of Tat‑Sab

Indexed as

LipopolysaccharidesRespiratory Distress SyndromeAnimalsApoptosisEndoplasmic Reticulum StressMiceMitochondriaLipopolysaccharidesacute lung injury and acute respiratory distress syndromec‑Jun‑N‑terminal kinaseendoplasmic reticulum stressmitochondria

Identifiers

PMID35514298
PMCPMC9106374
OpenAlexW4225414551

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.