Evidence map›Paper›PMID 35493086›Full record

ReviewFrontiers in cell and developmental biology2022

NLRP3-Mediated Inflammation in Atherosclerosis and Associated Therapeutics.

Na Lu, Weijia Cheng, Dongling Liu, Gang Liu, Can Cui, Chaoli Feng, Xianwei Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 6% 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, 42 citations in OpenAlex.

  1. Article
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  3. IGF2BP1 modulates ZDHHC5-mediated NLRP3 inflammasome activation to promote mitochondrial damage and foam cell formation of vascular smooth muscle cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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 at 2 institutions in 1 country.

Na LuHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Weijia ChengHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Dongling LiuHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Gang LiuHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Can CuiHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Chaoli FengHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Xianwei WangHenan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Xinxiang Medical University · CNFirst Affiliated Hospital of Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome is a crucial constituent of the body's innate immune system, and a multiprotein platform which is initiated by pattern recognition receptors (PRRs). Its activation leads to caspase-1 maturation and release of inflammatory cytokines, interleukin-1β (IL-1β) and IL-18, and subsequently causes pyroptosis. Recently, the excess activation of NLRP3 inflammasome has been confirmed to mediate inflammatory responses and to participate in genesis and development of atherosclerosis. Therefore, the progress on the discovery of specific inhibitors against the NLRP3 inflammasome and the upstream and downstream inflammatory factors has become potential targets for clinical treatment. Here we review the recently described mechanisms about the NLRP3 inflammasome activation, and discuss emphatically the pharmacological interventions using statins and natural medication for atherosclerosis associated with NLRP3 inflammasome.

Indexed as

atherosclerosisinflammationmechanismNLRP3 inflammasometherapeutics

Identifiers

PMID35493086
PMCPMC9045366
OpenAlexW4223934345

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.