Evidence map›Paper›PMID 29531021›Full record

ArticleEMBO molecular medicine2018

Tranilast directly targets NLRP3 to treat inflammasome-driven diseases.

Yi Huang, Hua Jiang, Yun Chen, Xiaqiong Wang, Yanqing Yang, Jinhui Tao, Xianming Deng, Gaolin Liang, Huafeng Zhang, Wei Jiang and 1 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 290 papers.

0numbers the graph read from it
0cells of the map it votes in
290citing papers in PubMed
15.7field-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

290 citing papers in PubMed, 485 citations in OpenAlex.

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230 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

11 authors at 3 institutions in 1 country.

Yi HuangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China.
Hua JiangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China.
Yun ChenState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, China.
Xiaqiong WangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China.
Yanqing YangDepartment of Clinical Laboratory, The First Affiliated Hospital of Bengbu Medical College, Bengbu, China.
Jinhui TaoDepartment of Rheumatology & Immunology, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, China.
Xianming DengState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, China.
Gaolin LiangCAS Key Laboratory of Soft Matter Chemistry, Department of Chemistry, University of Science and Technology of China, Hefei, China.
Huafeng ZhangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China.ORCID 0000-0001-9923-7531
Wei JiangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China ustcjw@ustc.edu.cn zrb1980@ustc.edu.cn.ORCID 0000-0001-8327-3079
Rongbin ZhouInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China ustcjw@ustc.edu.cn zrb1980@ustc.edu.cn.ORCID 0000-0002-3351-6420
University of Science and Technology of China · CNXiamen University · CNFirst Affiliated Hospital of Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dysregulation of NLRP3 inflammasome can cause uncontrolled inflammation and drive the development of a wide variety of human diseases, but the medications targeting NLRP3 inflammasome are not available in clinic. Here, we show that tranilast (TR), an old anti-allergic clinical drug, is a direct NLRP3 inhibitor. TR inhibits NLRP3 inflammasome activation in macrophages, but has no effects on AIM2 or NLRC4 inflammasome activation. Mechanismly, TR directly binds to the NACHT domain of NLRP3 and suppresses the assembly of NLRP3 inflammasome by blocking NLRP3 oligomerization.

Indexed as

AnimalsChloridesDNA-Binding ProteinsEnzyme-Linked Immunosorbent AssayHEK293 CellsHumansImmunoprecipitationInflammasomesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 Proteinortho-AminobenzoatesPotassiumAIM2 protein, humanChloridesDNA-Binding ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 Proteinortho-AminobenzoatesPotassiumtranilastdirectly bindinflammasome‐driven diseasesinhibitorNLRP3tranilast

Identifiers

PMID29531021
PMCPMC5887903
OpenAlexW2790572647

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.