Evidence map›Paper›PMID 28690868›Full record

ArticleCell discovery2017

miRNA-200c-3p is crucial in acute respiratory distress syndrome.

Qiang Liu, Jianchao Du, Xuezhong Yu, Jun Xu, Fengming Huang, Xiaoyun Li, Cong Zhang, Xiao Li, Jiahui Chang, Daozhen Shang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

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  20. Non-coding RNA in SARS-CoV-2: Progress toward therapeutic significance.International journal of biological macromolecules · 2022
    Review

20 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

18 authors at 3 institutions in 1 country.

Qiang LiuDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.ORCID 0000-0002-6343-8080
Jianchao DuDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Xuezhong YuDepartment of Emergency, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Jun XuDepartment of Emergency, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Fengming HuangDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Xiaoyun LiDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Cong ZhangSchool of Life Science, University of Science and Technology of China, Hefei, China.
Xiao LiGenetic Engineering Laboratory, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.
Jiahui ChangDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Daozhen ShangDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Yan ZhaoDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Mingyao TianGenetic Engineering Laboratory, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.
Huijun LuGenetic Engineering Laboratory, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.
Jiantao XuDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Chang LiGenetic Engineering Laboratory, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.
Huadong ZhuDepartment of Emergency, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Ningyi JinGenetic Engineering Laboratory, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China.
Chengyu JiangDepartment of Biochemistry, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNAcademy of Military Medical Sciences · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza infection and pneumonia are known to cause much of their mortality by inducing acute respiratory distress syndrome (ARDS), which is the most severe form of acute lung injury (ALI). Angiotensin-converting enzyme 2 (ACE2), which is a negative regulator of angiotensin II in the renin-angiotensin system, has been reported to have a crucial role in ALI. Downregulation of ACE2 is always associated with the ALI or ARDS induced by avian influenza virus, severe acute respiratory syndrome-coronavirus, respiratory syncytial virus and sepsis. However, the molecular mechanism of the decreased expression of ACE2 in ALI is unclear. Here we show that avian influenza virus H5N1 induced the upregulation of miR-200c-3p, which was then demonstrated to target the 3'-untranslated region of ACE2. Then, we found that nonstructural protein 1 and viral RNA of H5N1 contributed to the induction of miR-200c-3p during viral infection. Additionally, the synthetic analog of viral double-stranded RNA (poly (I:C)), bacterial lipopolysaccharide and lipoteichoic acid can all markedly increase the expression of miR-200c-3p in a nuclear factor

Indexed as

angiotensininfluenzaLPSLTAmiRNApneumoniapoly (I:C)

Identifiers

PMID28690868
PMCPMC5485385
OpenAlexW2733455360

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.