Evidence map›Paper›PMID 29928282›Full record

ReviewFrontiers in immunology2018

IRE1α Implications in Endoplasmic Reticulum Stress-Mediated Development and Pathogenesis of Autoimmune Diseases.

Raghu Patil Junjappa, Prakash Patil, Kashi Raj Bhattarai, Hyung-Ryong Kim, Han-Jung Chae

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

82 citing papers in PubMed, 115 citations in OpenAlex.

  1. Review
  2. Metabolites · 2026
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  11. International journal of molecular sciences · 2026
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22 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Raghu Patil JunjappaDepartment of Pharmacology, School of Medicine, Institute of New Drug Development, Chonbuk National University, Jeonju, South Korea.
Prakash PatilDepartment of Pharmacology, School of Medicine, Institute of New Drug Development, Chonbuk National University, Jeonju, South Korea.
Kashi Raj BhattaraiDepartment of Pharmacology, School of Medicine, Institute of New Drug Development, Chonbuk National University, Jeonju, South Korea.
Hyung-Ryong KimGraduate School, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu, South Korea.
Han-Jung ChaeDepartment of Pharmacology, School of Medicine, Institute of New Drug Development, Chonbuk National University, Jeonju, South Korea.
Jeonbuk National University · KRDaegu Gyeongbuk Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α) is the most prominent and evolutionarily conserved endoplasmic reticulum (ER) membrane protein. This transduces the signal of misfolded protein accumulation in the ER, named as ER stress, to the nucleus as "unfolded protein response (UPR)." The ER stress-mediated IRE1α signaling pathway arbitrates the yin and yang of cell life. IRE1α has been implicated in several physiological as well as pathological conditions, including immune disorders. Autoimmune diseases are caused by abnormal immune responses that develop due to genetic mutations and several environmental factors, including infections and chemicals. These factors dysregulate the cell immune reactions, such as cytokine secretion, antigen presentation, and autoantigen generation. However, the mechanisms involved, in which these factors induce the onset of autoimmune diseases, are remaining unknown. Considering that these environmental factors also induce the UPR, which is expected to have significant role in secretory cells and immune cells. The role of the major UPR molecule, IRE1α, in causing immune responses is well identified, but its role in inducing autoimmunity and the pathogenesis of autoimmune diseases has not been clearly elucidated. Hence, a better understanding of the role of IRE1α and its regulatory mechanisms in causing autoimmune diseases could help to identify and develop the appropriate therapeutic strategies. In this review, we mainly center the discussion on the molecular mechanisms of IRE1α in the pathophysiology of autoimmune diseases.

Indexed as

Disease SusceptibilityEndoplasmic Reticulum StressAnimalsApoptosisAutoimmune DiseasesAutoimmunityBiomarkersEndoplasmic ReticulumEndoribonucleasesHumansInflammationProtein Serine-Threonine KinasesSignal TransductionBiomarkersEndoribonucleasesERN1 protein, humanProtein Serine-Threonine Kinasesautoimmune diseasescytokinesinflammationIRE1αregulated IRE1α-dependent decayunfolded protein response signaling pathways

Identifiers

PMID29928282
PMCPMC5997832
OpenAlexW2806777665

What OpenQuestion holds

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Registered trials

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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.