Evidence map›Paper›PMID 34992411›Full record

ReviewJournal of inflammation research2021

Spotlight on NLRP3 Inflammasome: Role in Pathogenesis and Therapies of Atherosclerosis.

Chunteng Jiang, Santuan Xie, Guang Yang, Ningning Wang

Open access · goldAbstract readReview
In one paragraph

Review in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Oxidized Low-Density Lipoprotein and Its Role in Immunometabolism.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Review
  12. Article
  13. Investigating the Effects of Sex Hormones on Macrophage Polarization.International journal of molecular sciences · 2024
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

4 authors at 2 institutions in 2 countries.

Chunteng JiangDepartment of Internal Medicine, The Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning, People's Republic of China.ORCID 0000-0001-6875-6021
Santuan XieDepartment of Internal Medicine, The Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning, People's Republic of China.
Guang YangDepartment of Food Nutrition and Safety, School of Public Health, Dalian Medical University, Dalian, Liaoning, People's Republic of China.
Ningning WangDepartment of Food Nutrition and Safety, School of Public Health, Dalian Medical University, Dalian, Liaoning, People's Republic of China.ORCID 0000-0001-7883-4556
Affiliated Zhongshan Hospital of Dalian University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is an intricate biological response of body tissues to detrimental stimuli. Cardiovascular disease (CVD) is the leading cause of death worldwide, and inflammation is well documented to play a role in the development of CVD, especially atherosclerosis (AS). Emerging evidence suggests that activation of the NOD-like receptor (NLR) family and the pyridine-containing domain 3 (NLRP3) inflammasome is instrumental in inflammation and may result in AS. The NLRP3 inflammasome acts as a molecular platform that triggers the activation of caspase-1 and the cleavage of pro-interleukin (IL)-1β, pro-IL-18, and gasdermin D (GSDMD). The cleaved GSDMD forms pores in the cell membrane and initiates pyroptosis, inducing cell death and the discharge of intracellular pro-inflammatory factors. Hence, the NLRP3 inflammasome is a promising target for anti-inflammatory therapy against AS. In this review, we systematically summarized the current understanding of the activation mechanism of NLRP3 inflammasome, and the pathological changes in AS involving NLRP3. We also discussed potential therapeutic strategies targeting NLRP3 inflammasome to combat AS.

Indexed as

atherosclerosiscardiovascular diseasemechanismsNLRP3 inflammasometherapeutic strategies

Identifiers

PMID34992411
PMCPMC8711145
OpenAlexW4200417648

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.