Evidence map›Paper›PMID 30186288›Full record

ArticleFrontiers in immunology2018

Repositioning of the β-Blocker Carvedilol as a Novel Autophagy Inducer That Inhibits the NLRP3 Inflammasome.

Wei-Ting Wong, Lan-Hui Li, Yerra Koteswara Rao, Shih-Ping Yang, Shu-Meng Cheng, Wen-Yu Lin, Cheng-Chung Cheng, Ann Chen, Kuo-Feng Hua

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-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

43 citing papers in PubMed, 66 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Wei-Ting WongNational Defense Medical Center, Graduate Institute of Life Sciences, Taipei, Taiwan.
Lan-Hui LiDepartment of Laboratory Medicine, Linsen, Chinese Medicine and Kunming Branch, Taipei City Hospital, Taipei, Taiwan.
Yerra Koteswara RaoDepartment of Biotechnology and Animal Science, National Ilan University, Yilan City, Taiwan.
Shih-Ping YangDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Shu-Meng ChengDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Wen-Yu LinDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Cheng-Chung ChengDivision of Cardiology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Ann ChenDepartment of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Kuo-Feng HuaDepartment of Biotechnology and Animal Science, National Ilan University, Yilan City, Taiwan.
National Defense Medical Center · TWTri-Service General Hospital · TWNational Ilan University · TWTaipei City Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome is a multiprotein complex that plays a key role in the innate immune system, and aberrant activation of this complex is involved in the pathogenesis of inflammatory diseases. Carvedilol (CVL) is an α-, β-blocker used to treat high blood pressure and congestive heart failure; however, some benefits beyond decreased blood pressure were observed clinically, suggesting the potential anti-inflammatory activity of CVL. In this report, the inhibitory potential of CVL toward the NLRP3 inflammasome and the possible underlying molecular mechanisms were studied. Our results showed that CVL attenuated NLRP3 inflammasome activation and pyroptosis in mouse macrophages, without affecting activation of the AIM2, NLRC4 and non-canonical inflammasomes. Mechanistic analysis revealed that CVL prevented lysosomal and mitochondrial damage and reduced ASC oligomerization. Additionally, CVL caused autophagic induction through a Sirt1-dependent pathway, which inhibited the NLRP3 inflammasome. In the

Indexed as

Adrenergic beta-AntagonistsAnimalsAutophagyCarvedilolCell LineCytokinesDisease Models, AnimalInflammasomesMacrophages, PeritonealMaleMiceNLR Family, Pyrin Domain-Containing 3 ProteinPeritonitisPyroptosisAdrenergic beta-AntagonistsCarvedilolCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseautophagyCarvedilolmitochondriaNLRP3 inflammasomeperitonitis

Identifiers

PMID30186288
PMCPMC6113403
OpenAlexW2888753367

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.