Evidence map›Paper›PMID 31607947›Full record

ArticleFrontiers in physiology2019

The IRE1α Arm of UPR Regulates Muscle Cells Immune Characters by Restraining p38 MAPK Activation.

RuiCai Gu, Tao Huang, JiangWei Xiao, ZhaoHong Liao, JunHua Li, HaiQiang Lan, Jun Ouyang, JiJie Hu, Hua Liao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

9 authors at 1 institution in 1 country.

RuiCai GuGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Tao HuangGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
JiangWei XiaoGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
ZhaoHong LiaoGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
JunHua LiGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
HaiQiang LanGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Jun OuyangGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
JiJie HuDepartment of Orthopaedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hua LiaoGuangdong Provincial Key Laboratory of Medical Biomechanics, Department of Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle repair and systemic inflammation/immune responses are linked to endoplasmic reticulum stress (ER stress) pathways in myopathic muscle, and muscle cells play an active role in muscular immune reactions by exhibiting immunological characteristics under persistent proinflammation stimuli. Whether ER stress affects the intrinsic immunological capacities of myocytes in the inflammatory milieu, as it does to immune cells, and which arms of the unfolded protein response (UPR) mainly participate in these processes remain mostly unknown. We investigated this issue and showed that inflammatory stimuli can induce the activation of the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) and inositol-requiring enzyme 1α (IRE1α) arms of the UPR in myocytes both

Indexed as

endoplasmic reticulum stressinositol-requiring enzyme 1αmyotubesp38 MAPKunfolded protein responses

Identifiers

PMID31607947
PMCPMC6761248
OpenAlexW2971541913

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.