Evidence map›Paper›PMID 35503561›Full record

ArticleZoological research2022

Combinational benefit of antihistamines and remdesivir for reducing SARS-CoV-2 replication and alleviating inflammation-induced lung injury in mice.

Meng-Li Wu, Feng-Liang Liu, Jing Sun, Xin Li, Jian-Ru Qin, Qi-Hong Yan, Xia Jin, Xin-Wen Chen, Yong-Tang Zheng, Jin-Cun Zhao and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Zoological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 8 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

11 authors at 3 institutions in 1 country.

Meng-Li WuCollege of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
Feng-Liang LiuKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China.
Jing SunState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510182, China.
Xin LiGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong 510530, China.
Jian-Ru QinCollege of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
Qi-Hong YanState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510182, China.
Xia JinCollege of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
Xin-Wen ChenGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong 510530, China.
Yong-Tang ZhengKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China. E-mail: zhengyt@mail.kiz.ac.cn.
Jin-Cun ZhaoState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510182, China. E-mail: zhaojincun@gird.cn.
Jian-Hua WangGuangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong 510530, China.
Chinese Academy of Sciences · CNKunming Institute of Zoology · CNFirst Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 is an immune-mediated inflammatory disease caused by SARS-CoV-2 infection, the combination of anti-inflammatory and antiviral therapy is predicted to provide clinical benefits. We recently demonstrated that mast cells (MCs) are an essential mediator of SARS-CoV-2-initiated hyperinflammation. We also showed that spike protein-induced MC degranulation initiates alveolar epithelial inflammation for barrier disruption and suggested an off-label use of antihistamines as MC stabilizers to block degranulation and consequently suppress inflammation and prevent lung injury. In this study, we emphasized the essential role of MCs in SARS-CoV-2-induced lung lesions

Indexed as

COVID-19COVID-19 Drug TreatmentLung InjuryAdenosine MonophosphateAlanineAnimalsAntiviral AgentsEndothelial CellsHistamine AntagonistsInflammationMiceSARS-CoV-2Spike Glycoprotein, CoronavirusAdenosine MonophosphateAlanineAntiviral AgentsHistamine AntagonistsremdesivirSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2AntihistamineCombinational therapyMast cellRemdesivirSARS-CoV-2

Identifiers

PMID35503561
PMCPMC9113965
OpenAlexW4225395150

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.