Evidence map›Paper›PMID 32447438›Full record

ReviewApplied microbiology and biotechnology2020

Crosstalk between ER stress, NLRP3 inflammasome, and inflammation.

Wei Li, Ting Cao, Chunyi Luo, Jialun Cai, Xiangping Zhou, Xinhua Xiao, Shuangquan Liu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Applied microbiology and biotechnology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
–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

166 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  18. Molecular medicine reports · 2026
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106 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

7 authors.

Wei LiDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Ting CaoDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Chunyi LuoDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Jialun CaiDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Xiangping ZhouDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Xinhua XiaoDepartment of Endocrinology, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China. xinhua0102@163.com.
Shuangquan LiuDepartment of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China. dantelliu@163.com.

Funding

Major special projects of Hunan Provincial Health and Family Planning Commission A2017011National Natural Science Foundation of China 81201331
6 · The paper itself

Abstract

Endoplasmic reticulum stress (ERS) is a protective response to restore protein homeostasis by activating the unfolded protein response (UPR). However, UPR can trigger cell death under severe and/or persistently high ERS. The NLRP3 inflammasome is a complex of multiple proteins that activates the secretion of the proinflammatory cytokine IL-1β in a caspase-1-dependent manner to participate in the regulation of inflammation. The NLRP3 inflammasome involvement in ERS-induced inflammation has not been completely described. The intersection of ERS with multiple inflammatory pathways can initiate and aggravate chronic diseases. Accumulating evidence suggests that ERS-induced activation of NLRP3 inflammasome is the pathological basis of various inflammatory diseases. In this review, we have discussed the networks between ERS and NLRP3 inflammasome, with the view to identifying novel therapeutic targets in inflammatory diseases. KEY POINTS: • Endoplasmic reticulum stress (ERS) is an important factor for the activation of the NLRP3 inflammasomes that results in pathological processes. • ERS can activate the NLRP3 inflammasome to induce inflammatory responses via oxidative stress, calcium homeostasis, and NF-κB activation. • The interactions between ERS and NLRP3 inflammasome are associated with inflammation, which represent a potential therapeutic opportunity of inflammatory diseases.

Indexed as

Endoplasmic Reticulum StressAnimalsCalciumHumansInflammasomesInflammationNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressProteostasisSignal TransductionUnfolded Protein ResponseCalciumInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinEndoplasmic reticulum stressInflammationNF-κBNLRP3 inflammasomeReactive oxygen species

Identifiers

PMID32447438

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.