Evidence map›Paper›PMID 32508013›Full record

ReviewClinical and translational medicine2020

NLRP3 inflammasome, an immune-inflammatory target in pathogenesis and treatment of cardiovascular diseases.

Yucheng Wang, Xiaoxiao Liu, Hui Shi, Yong Yu, Ying Yu, Minghui Li, Ruizhen Chen

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 2 pooled it
10.2field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 2 syntheses or guidelines pooled it, 197 citations in OpenAlex.

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  4. Theaflavin attenuates atherosclerosis by targeting GSK-3β to suppress pyroptosis and Promote Autophagy in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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55 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 at 1 institution in 1 country.

Yucheng WangDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Shanghai Medical College of Fudan University, Shanghai, China.
Xiaoxiao LiuDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Shanghai Medical College of Fudan University, Shanghai, China.
Hui ShiDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Shanghai Medical College of Fudan University, Shanghai, China.
Yong YuDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Shanghai Medical College of Fudan University, Shanghai, China.
Ying YuDepartment of General Practice, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Minghui LiDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Shanghai Medical College of Fudan University, Shanghai, China.
Ruizhen ChenDepartment of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Shanghai Medical College of Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-0333-2695
Shanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China 81521001National Natural Science Foundation of China 81671937National Natural Science Foundation of China 81772109
6 · The paper itself

Abstract

Inflammation is an important process involved in several cardiovascular diseases (CVDs), and nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a vital player in innate immunity and inflammation. In this review, we aim to provide a comprehensive summary of the current knowledge on the role and involvement of NLRP3 inflammasome in the pathogenesis and treatment of CVDs. NLRP3 inflammasome functions as a molecular platform, and triggers the activation of caspase-1 and cleavage of pro-IL-1β, pro-IL-18, and gasdermin D (GSDMD). Cleaved NT-GSDMD forms pores in the cell membrane and initiates pyroptosis, inducing cell death and release of many intracellular pro-inflammatory molecules. NLRP3 inflammasome activation is triggered via inter-related pathways downstream of K

Indexed as

atherosclerosisheart failureinflammationischemia/reperfusion injuryNLRP3 inflammasome

Identifiers

PMID32508013
PMCPMC7240865
OpenAlexW3019221417

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.