Evidence map›Paper›PMID 39747803›Full record

ArticleVirus genes2025

Long non-coding RNA C1RL-AS1 aggravates influenza A virus pneumonia through miR-16-5p/LAMP3.

Xingjuan Liao, Qin Liang, Chao Xu, Xinbing Luo

Abstract read
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In one paragraph

Article in Virus genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Review
4 · The record

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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

4 authors.

Xingjuan Liao *Department of Pediatrics, Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, No.32, Renmin South Road, Shiyan, 442000, China.
Qin Liang *Department of Pediatrics, Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, No.32, Renmin South Road, Shiyan, 442000, China.
Chao XuDepartment of Pediatrics, Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, No.32, Renmin South Road, Shiyan, 442000, China.
Xinbing LuoDepartment of Pediatrics, Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, No.32, Renmin South Road, Shiyan, 442000, China. luoxinbingdr@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza A viruses continue to pose a serious threat to public health and economic stability. To investigate the role of C1RL-AS1 in influenza A virus (IAV) pneumonia. Using RT-qPCR analysis, we determined C1RL-AS1 expression levels in children with IAV-infected pneumonia and A549 cells. C1RL-AS1 expression levels in children were subjected to ROC analysis. C1RL-AS1 was knocked down to investigate its role in IAV-infected A549 cells, including effects on viral nucleoprotein (NP) production, cell survival, and apoptosis. Downstream miRNAs of C1RL-AS1 were predicted and validated. MiR-16-5p target genes were predicted and validated. C1RL-AS1 was up-regulated in IAV-infected children and A549 cells. C1RL-AS1 expression levels distinguished children with IAV pneumonia from healthy children. Knockdown of C1RL-AS1 attenuated viral NP production, promoted A549 cell survival, and inhibited apoptosis. MiR-16-5p was a downstream C1RL-AS1 miRNA. miR-16-5p counteracted the anti-IAV infection effect brought about by C1RL-AS1 knockdown. LAMP3 was a miR-16-5p target gene associated with pneumonia. LAMP3 restored the cellular effects brought about by C1RL-AS1/miR-16-5p co-knockdown. C1RL-AS1 is a possible diagnostic factor for IAV pneumonia in children. C1RL-AS1 may participate in IAV pneumonia by sponging miR-16-5p and then moderating LAMP3.

Indexed as

Influenza A virusInfluenza, HumanMicroRNAsPneumonia, ViralRNA, Long NoncodingA549 CellsApoptosisChildChild, PreschoolFemaleHumansMaleVirus ReplicationMicroRNAsMIRN16 microRNA, humanRNA, Long NoncodingC1RL-AS1Influenza A virusLAMP3PneumoniaRespiratory failure

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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.