Evidence map›Paper›PMID 31767975›Full record

ArticleCellular & molecular immunology2021

MicroRNA-33/33* inhibit the activation of MAVS through AMPK in antiviral innate immunity.

Danhui Liu, Qinchun Tan, Jie Zhu, Yuanyuan Zhang, Yue Xue, Yinjing Song, Yang Liu, Qingqing Wang, Lihua Lai

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Lnc90386 Sponges miR-33-5p to MediateFrontiers in immunology · 2022
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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 3 institutions in 1 country.

Danhui Liu *Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Qinchun Tan *Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Jie Zhu *Department of Clinical Laboratory, Zhejiang Hospital, Hangzhou, 310030, China.
Yuanyuan ZhangThe Children's Hospital of Zhejiang University School of Medicine, Hangzhou, 310052, China.
Yue XueInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Yinjing SongInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Yang LiuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China. wqq@zju.edu.cn.
Lihua LaiInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, China. lailihua@zju.edu.cn.ORCID http://orcid.org/0000-0003-1459-018X
Zhejiang University · CNChildren's Hospital of Zhejiang University · CNZhejiang Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81401283National Natural Science Foundation of China (National Science Foundation of China) 81771699Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LY15C080001Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LY18H100004Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LZ19H100001
6 · The paper itself

Abstract

Innate immunity plays a prominent role in the host defense against pathogens and must be precisely regulated. As vital orchestrators in cholesterol homeostasis, microRNA-33/33* have been widely investigated in cellular metabolism. However, their role in antiviral innate immunity is largely unknown. Here, we report that VSV stimulation decreased the expression of miR-33/33* through an IFNAR-dependent manner in macrophages. Overexpression of miR-33/33* resulted in impaired RIG-I signaling, enhancing viral load and lethality whereas attenuating type I interferon production both in vitro and in vivo. In addition, miR-33/33* specifically prevented the mitochondrial adaptor mitochondrial antiviral-signaling protein (MAVS) from forming activated aggregates by targeting adenosine monophosphate activated protein kinase (AMPK), subsequently impeding the mitophagy-mediated elimination of damaged mitochondria and disturbing mitochondrial homeostasis which is indispensable for efficient MAVS activation. Our findings establish miR-33/33* as negative modulators of the RNA virus-triggered innate immune response and identify a previously unknown regulatory mechanism linking mitochondrial homeostasis with antiviral signaling pathways.

Indexed as

Immunity, InnateAdaptor Proteins, Signal TransducingAdenylate KinaseAnimalsAntagomirsBase SequenceDEAD Box Protein 58Down-RegulationGene SilencingHEK293 CellsHeLa CellsHumansInterferon Type IMacrophagesMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingAdenylate KinaseAntagomirsDEAD Box Protein 58IFNAR1 protein, humanInterferon Type IMAVS protein, humanMicroRNAsMIRN33a microRNA, humanProtein AggregatesReceptor, Interferon alpha-betaReceptors, ImmunologicRIGI protein, humanAMPKαMAVSmicroRNA-33/33*mitophagytype I interferon

Identifiers

PMID31767975
PMCPMC8167167
OpenAlexW2990830202

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.