Evidence map›Paper›PMID 36882503›Full record

ArticleActa pharmacologica Sinica2023

Celastrol attenuates hepatitis C virus translation and inflammatory response in mice by suppressing heat shock protein 90β.

Shao-Ru Chen, Zheng-Qing Li, Jun Xu, Mo-Yu Ding, Ya-Ming Shan, Yung-Chi Cheng, Gao-Xiao Zhang, Ye-Wei Sun, Yu-Qiang Wang, Ying Wang

Open access · greenAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  6. The role of celastrol in inflammation and diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
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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

10 authors at 6 institutions in 4 countries.

Shao-Ru ChenInstitute of Chinese Medical Sciences and State Key Laboratory of Quality Research in Chinese Medicine, University of Macau, Macao SAR, China.
Zheng-Qing LiInstitute of Chinese Medical Sciences and State Key Laboratory of Quality Research in Chinese Medicine, University of Macau, Macao SAR, China.
Jun XuResearch Center for Drug Discovery, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, 510006, China.
Mo-Yu DingInstitute of Chinese Medical Sciences and State Key Laboratory of Quality Research in Chinese Medicine, University of Macau, Macao SAR, China.
Ya-Ming ShanNational Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, 130012, China.
Yung-Chi ChengDepartment of Pharmacology, Yale University, New Haven, CT, 06510, USA.
Gao-Xiao ZhangInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou, 510632, China.
Ye-Wei SunInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou, 510632, China.
Yu-Qiang WangInstitute of New Drug Research and Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine, Jinan University College of Pharmacy, Guangzhou, 510632, China.
Ying WangInstitute of Chinese Medical Sciences and State Key Laboratory of Quality Research in Chinese Medicine, University of Macau, Macao SAR, China. emilyywang@um.edu.mo.
Jinan University · CNUniversity of Macau · MOCSSC Offshore & Marine Engineering Company (China) · CNJilin University · CNSun Yat-sen University · CNYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is one of the major factors to trigger a sustained hepatic inflammatory response and hence hepatocellular carcinoma (HCC), but direct-acting-antiviral (DAAs) was not efficient to suppress HCC development. Heat shock protein 90 kDa (HSP90) is highly abundant in different types of cancers, and especially controls protein translation, endoplasmic reticulum stress, and viral replication. In this study we investigated the correlation between the expression levels of HSP90 isoforms and inflammatory response marker NLRP3 in different types of HCC patients as well as the effect of a natural product celastrol in suppression of HCV translation and associated inflammatory response in vivo. We identified that the expression level of HSP90β isoform was correlated with that of NLRP3 in the liver tissues of HCV positive HCC patients (R

Indexed as

Carcinoma, HepatocellularHepatitis CLiver NeoplasmsAnimalsHeat-Shock ProteinsHepacivirusHSP90 Heat-Shock ProteinsInflammationMiceNLR Family, Pyrin Domain-Containing 3 ProteinPentacyclic TriterpenescelastrolHeat-Shock ProteinsHSP90 Heat-Shock ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinPentacyclic Triterpenescelastrolheat shock protein 90βhepatitis C virusinflammatory responseRNA-dependent RNA polymerase

Identifiers

PMID36882503
PMCPMC10374583
OpenAlexW4323362638

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.