Evidence map›Paper›PMID 32656610›Full record

ReviewInflammation2020

A Spotlight on the Underlying Activation Mechanisms of the NLRP3 Inflammasome and its Role in Atherosclerosis: A Review.

Anam Liaqat, Muhammad Asad, Fatima Shoukat, Arif-Ullah Khan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. NLRP3-Mediated Inflammation in Atherosclerosis and Associated Therapeutics.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. Review
  13. IntermedinCell death & disease · 2021
    Article
  14. Review
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 1 country.

Anam LiaqatRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, 44000, Pakistan. anamliaqat29@gmail.com.ORCID http://orcid.org/0000-0002-1849-8455
Muhammad AsadArmed Forces Institute of Cardiology, National Institute of Heart Diseases, Rawalpindi, Pakistan.
Fatima ShoukatRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, 44000, Pakistan.
Arif-Ullah KhanRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, 44000, Pakistan.
Riphah International University · PKArmed Forces Institute of Pathology · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The world's number one cause of death is cardiovascular diseases. The pathogenesis of different disease entities in the cardiovascular disease spectrum is complicated and multifactorial. Inflammation in these complicated etiologies serves as a key position and is a significant cause of atherosclerosis, which contributes to the underlying pathology. Therefore, therapeutic targeting of inflammatory pathways in patients with cardiovascular diseases such as atherosclerosis enhances cardiovascular results. Inflammasomes are intracellular protein complexes engaged in atherosclerosis pathogenesis and activated by multiple danger signals. Emerging proof has revealed that Nod-like receptor protein 3 (NLRP3) inflammasome, which regulates caspase-1 activation and later pro-interleukin processing, triggers inflammatory reactions in the vascular wall and leads to atherosclerotic plaque formation. Inflammasome-mediated signaling interference could decrease inflammation and mitigate illness severity. In this section, we provide an overview of the present literature on the underlying mechanisms leading to the activation of NLRP3 inflammasome and the role of NLRP3 inflammasome in the progression of atherogenesis and highlight the possibility of therapeutic interventions due to mechanisms involved in the of inhibition of NLRP3 activation.

Indexed as

AnimalsAtherosclerosisCaspase 1CytoplasmEndoplasmic Reticulum StressEndothelial CellsHumansInflammasomesInflammationInterleukin-18LysosomesMacrophagesMiceModels, BiologicalMyocytes, Smooth MuscleNLR Family, Pyrin Domain-Containing 3 ProteinCaspase 1InflammasomesInterleukin-18NLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanatherosclerosiscardiovascular diseaseinflammasomeinflammationinterleukin-1β

Identifiers

PMID32656610
OpenAlexW3043004764

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.