Evidence map›Paper›PMID 41208954›Full record

ReviewFrontiers in immunology2025

Endoplasmic reticulum stress and unfolded protein response in immune cell function.

Goshi Matsushima, Yuhki Yanase, Tadashi Nakagawa, Mitsuhiro Goda, Koichiro Ozawa, Toru Hosoi

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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.

Goshi MatsushimaDepartment of Clinical Pharmacology and Therapeutics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yuhki YanaseDepartment of Clinical Pharmacology and Therapeutics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Tadashi NakagawaDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University, Yamaguchi, Japan.
Mitsuhiro GodaDepartment of Clinical Pharmacology and Therapeutics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Koichiro OzawaDepartment of Clinical Pharmacology and Therapeutics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Toru HosoiDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University, Yamaguchi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) have emerged as central regulators of immune cell function and inflammatory processes. The UPR, mediated by three principal ER-resident sensors, IRE1α, PERK and ATF6, maintains cellular homeostasis under stress conditions but also contributes to pathogenesis when dysregulated. Recent studies revealed that the UPR plays critical roles not only in protein folding but also in directing immune cell fate, activation, and cytokine production. Although significant advances have been made, various questions remain regarding the cell-type-specific and context-dependent functions of ER stress responses. Understanding these mechanisms would be crucial for developing targeted therapies. Therefore, in this review, we provide a comprehensive overview of how ER stress and the UPR influence various immune cell types, including monocytes, macrophages, dendritic cells, granulocytes, T cells, B cells, microglia, and astrocytes, within both peripheral and central immune systems.

Indexed as

Endoplasmic Reticulum StressUnfolded Protein ResponseAnimalsHumansSignal TransductionATF6 (activating transcription factor 6)endoplasmic reticulum stressimmune cellsIRE1 (inositol-requiring enzyme 1)PERK (PKR-like endoplasmic reticulum kinase)unfolded protein response

Identifiers

PMID41208954
PMCPMC12592176

What Socratic 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 Socratic graph.