Evidence map›Paper›PMID 36171907›Full record

ArticleFrontiers in endocrinology2022

ER stress promotes mitochondrial DNA mediated type-1 interferon response in beta-cells and interleukin-8 driven neutrophil chemotaxis.

Saurabh Vig, Joost M Lambooij, Mette C Dekkers, Frank Otto, Françoise Carlotti, Bruno Guigas, Arnaud Zaldumbide

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. A surviving beta cell subpopulation enriched in patients with T1D.bioRxiv : the preprint server for biology · 2026
    Article
  4. Review
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  6. Defective RNA Polymerase III sensing of mitochondrial DNA in pulmonary epithelial cells impairs type I IFN immunity to SARS-CoV-2.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  16. The Activation of cGAS-STING in Acute Kidney Injury.Journal of inflammation research · 2023
    Review
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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

7 authors at 1 institution in 1 country.

Saurabh VigDepartment of Cell and Chemical Biology Leiden University Medical Center, Leiden, Netherlands.
Joost M LambooijDepartment of Cell and Chemical Biology Leiden University Medical Center, Leiden, Netherlands.
Mette C DekkersDepartment of Cell and Chemical Biology Leiden University Medical Center, Leiden, Netherlands.
Frank OttoDepartment of Parasitology, Leiden University Medical Center, Leiden, Netherlands.
Françoise CarlottiDepartment of Internal Medicine, Leiden University Medical Center, Leiden, Netherlands.
Bruno GuigasDepartment of Parasitology, Leiden University Medical Center, Leiden, Netherlands.
Arnaud ZaldumbideDepartment of Cell and Chemical Biology Leiden University Medical Center, Leiden, Netherlands.
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beta-cell destruction in type 1 diabetes (T1D) results from the combined effect of inflammation and recurrent autoimmunity. Accumulating evidence suggests the engagement of cellular stress during the initial stage of the disease, preceding destruction and triggering immune cell infiltration. While the role of the endoplasmic reticulum (ER) in this process has been largely described, the participation of the other cellular organelles, particularly the mitochondria which are central mediator for beta-cell survival and function, remains poorly investigated. Here, we have explored the contribution of ER stress, in activating type-I interferon signaling and innate immune cell recruitment. Using human beta-cell line EndoC-βH1 exposed to thapsigargin, we demonstrate that induction of cellular stress correlates with mitochondria dysfunction and a significant accumulation of cytosolic mitochondrial DNA (mtDNA) that triggers neutrophils migration by an IL8-dependent mechanism. These results provide a novel mechanistic insight on how ER stress can cause insulitis and may ultimately facilitate the identification of potential targets to protect beta-cells against immune infiltration.

Indexed as

DNA, MitochondrialEndoplasmic Reticulum StressInsulin-Secreting CellsInterferonsInterleukin-8ChemotaxisHumansMitochondriaNeutrophilsThapsigarginDNA, MitochondrialInterferonsInterleukin-8ThapsigarginER stressinnate immunitymitochondrianeutrophilstype 1 diabetes

Identifiers

PMID36171907
PMCPMC9511040
OpenAlexW4295235678

What OpenQuestion holds

Textmetadata
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.