Evidence map›Paper›PMID 36905430›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.

Yonghu Chen, Yuqi Zhang, Ning Li, Zhe Jiang, Xuezheng Li

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024
    Review
  13. Review
  14. Review
  15. Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024
    Review
  16. Article
  17. Review
  18. Article
  19. Article
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.

Yonghu ChenYanbian University Hospital, Yanbian University, Yanji, 133002, People's Republic of China.
Yuqi ZhangShenyang Pharmaceutical University, Shenyang, 110016, People's Republic of China.
Ning LiShenyang Pharmaceutical University, Shenyang, 110016, People's Republic of China.
Zhe JiangYanbian University Hospital, Yanbian University, Yanji, 133002, People's Republic of China. jiangz@ybu.edu.cn.
Xuezheng LiYanbian University Hospital, Yanbian University, Yanji, 133002, People's Republic of China. xzli@ybu.edu.cn.
Yanbian University Hospital · CNShenyang Pharmaceutical University · CN

Funding

Xuezheng Li 82260820Zhe Jiang 20200201034JC
6 · The paper itself

Abstract

backgroundAs an organelle essential for intracellular energy supply, mitochondria are involved in intracellular metabolism and inflammation, and cell death. The interaction of mitochondria with the NLRP3 inflammasome in the development of lung diseases has been extensively studied. However, the exact mechanism by which mitochondria mediate the activation of the NLRP3 inflammasome and trigger lung disease is still unclear.

methodsThe literatures related to mitochondrial stress, NLRP3 inflammasome and lung diseases were searched in PubMed.

resultsThis review aims to provide new insights into the recently discovered mitochondrial regulation of the NLRP3 inflammasome in lung diseases. It also describes the crucial roles of mitochondrial autophagy, long noncoding RNA, micro RNA, altered mitochondrial membrane potential, cell membrane receptors, and ion channels in mitochondrial stress and regulation of the NLRP3 inflammasome, in addition to the reduction of mitochondrial stress by nuclear factor erythroid 2-related factor 2 (Nrf2). The effective components of potential drugs for the treatment of lung diseases under this mechanism are also summarized.

conclusionThis review provides a resource for the discovery of new therapeutic mechanisms and suggests ideas for the development of new therapeutic drugs, thus promoting the rapid treatment of lung diseases.

Indexed as

InflammasomesLung DiseasesAutophagyHumansMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesLung diseasesMitochondriaNLRP3 inflammasomeOxidative stressPotential drugs

Identifiers

PMID36905430
PMCPMC10007669
OpenAlexW4323920704

What Socratic 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 Socratic graph.