Evidence map›Paper›PMID 36849929›Full record

ArticleCellular & molecular biology letters2023

IRE1α arm of unfolded protein response in muscle-specific TGF-β signaling-mediated regulation of muscle cell immunological properties.

Jiangwei Xiao, Jingwen Huang, Xiaoting Jian, Han Wang, Haiqiang Lan, Zhaohong Liao, Ruicai Gu, Jijie Hu, Hua Liao

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. [ENan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  4. Article
  5. 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

9 authors at 3 institutions in 2 countries.

Jiangwei Xiao *Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Jingwen Huang *Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.ORCID http://orcid.org/0000-0002-2705-7803
Xiaoting JianGuangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Han WangGuangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Haiqiang LanGuangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Zhaohong LiaoGuangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Ruicai GuDepartment of Cell Biology, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
Jijie HuDepartment of Orthopaedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. hjj0610@163.com.
Hua LiaoGuangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Anatomy, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China. hua-liao@163.com.
Southern Medical University · CNNanfang Hospital · CNUniversity of Oklahoma Health Sciences Center · US

Funding

Guangzhou Municipal Science and Technology Project 202002030497Key Programme 2022YFF1202600National Natural Science Foundation of China 32071181Natural Science Foundation of Guangdong Province 2021A1515010010
6 · The paper itself

Abstract

Endoplasmic reticulum stress (ERS) and the unfolded protein response (UPR) are involved in various muscle pathological states. The IRE1α arm of UPR can affect immunological properties of myofiber through restraining p38 mitogen-activated protein kinases (MAPK) activation under inflammatory milieu. However, the relevant pathway molecules regulating the initiation of the IRE1α arm in myofiber remain unclear. In this work, expression of transforming growth factor-beta (TGF-β) and TGF-β receptor II (TGF-βr2), and UPR pathway activation were examined in cardiotoxin (CTX)-damaged mouse muscle, which revealed the activation of TGF-β signaling and UPR in CTX-damaged muscle and in regenerating myofibers. Using control or transgenic mice with TGF-βr2 deleted in skeletal muscle (SM TGF-βr2

Indexed as

EndoribonucleasesProtein Serine-Threonine KinasesAnimalsMiceMice, TransgenicMuscle CellsMuscle, Skeletalp38 Mitogen-Activated Protein KinasesTransforming Growth Factor betaUnfolded Protein ResponseEndoribonucleasesp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesTransforming Growth Factor betaInflammationIRE1αMyofiberp38 MAPKTGF-βUPR

Identifiers

PMID36849929
PMCPMC9972623
OpenAlexW4322493291

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.