Evidence map›Paper›PMID 31687078›Full record

ReviewOxidative medicine and cellular longevity2019

ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis.

Xinnong Chen, Xiaochen Guo, Qihui Ge, Yixuan Zhao, Huaiyu Mu, Junping Zhang

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
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  5. EnterotoxigenicBiology · 2025
    Article
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  8. Cigarette smoking induces NLRP3 inflammasome activation in patients with atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2025
    Article
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29 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

6 authors at 1 institution in 1 country.

Xinnong ChenFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.ORCID https://orcid.org/0000-0003-3010-4487
Xiaochen GuoFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.ORCID https://orcid.org/0000-0002-7376-7988
Qihui GeFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.ORCID https://orcid.org/0000-0001-6694-9671
Yixuan ZhaoFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.ORCID https://orcid.org/0000-0002-5915-910X
Huaiyu MuFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
Junping ZhangFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.ORCID https://orcid.org/0000-0002-7271-8615
First Teaching Hospital of Tianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endoplasmic reticulum (ER) is an important organelle that regulates several fundamental cellular processes, and ER dysfunction has implications for many intracellular events. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is an intracellularly produced macromolecular complex that can trigger pyroptosis and inflammation, and its activation is induced by a variety of signals. ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation. Intriguingly, the role of ER stress in inflammasome activation has not attracted a great deal of attention. In addition, increasing evidence highlights that both ER stress and NLRP3 inflammasome activation contribute to atherosclerosis (AS). AS is a common cardiovascular disease with complex pathogenesis, and the precise mechanisms behind its pathogenesis remain to be determined. Both ER stress and the NLRP3 inflammasome have emerged as critical individual contributors of AS, and owing to the multiple associations between these two events, we speculate that they contribute to the mechanisms of pathogenesis in AS. In this review, we aim to summarize the molecular mechanisms of ER stress, NLRP3 inflammasome activation, and the cross talk between these two pathways in AS in the hopes of providing new pharmacological targets for AS treatment.

Indexed as

Endoplasmic Reticulum StressAnimalsAtherosclerosisHomeostasisHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionInflammasomesNLR Family, Pyrin Domain-Containing 3 Protein

Identifiers

PMID31687078
PMCPMC6800950
OpenAlexW2978410399

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.