Evidence map›Paper›PMID 35108097›Full record

ArticleJournal of virology2022

MicroRNA 573 Rescues Endothelial Dysfunction during Dengue Virus Infection under PPARγ Regulation.

Shefali Banerjee, Chin Wei Xin, Justin Jang Hann Chu

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Observational
  3. Article
  4. Review
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

3 authors at 2 institutions in 2 countries.

Shefali BanerjeeDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA.
Chin Wei XinDepartment of Microbiology and Immunology, National University of Singapore, Singapore.
Justin Jang Hann ChuDepartment of Microbiology and Immunology, National University of Singapore, Singapore.ORCID 0000-0002-1673-6819
National University of Singapore · SGThe University of Texas Medical Branch at Galveston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early prognosis of abnormal vasculopathy is essential for effective clinical management of patients with severe dengue. An exaggerated interferon (IFN) response and release of vasoactive factors from endothelial cells cause vasculopathy. This study shows that dengue virus 2 (DENV2) infection of human umbilical vein endothelial cells (HUVEC) results in differentially regulated microRNAs (miRNAs) important for endothelial function. miR-573 was significantly downregulated in DENV2-infected HUVEC due to decreased peroxisome proliferator activator receptor gamma (PPARγ) activity. Restoring miR-573 expression decreased endothelial permeability by suppressing the expression of vasoactive angiopoietin 2 (ANGPT2). We also found that miR-573 suppressed the proinflammatory IFN response through direct downregulation of Toll-like receptor 2 (TLR2) expression. Our study provides a novel insight into miR-573-mediated regulation of endothelial function during DENV2 infection, which can be further translated into a potential therapeutic and prognostic agent for severe dengue patients.

Indexed as

Dengue VirusEndothelium, VascularMicroRNAsPPAR gammaSevere DengueAngiopoietin-2HumansHuman Umbilical Vein Endothelial CellsAngiopoietin-2ANGPT2 protein, humanMicroRNAsMIRN573 microRNA, humanPPAR gammadengue feverendothelial permeabilitymiR-573PPARs

Identifiers

PMID35108097
PMCPMC8941877
OpenAlexW4220983714

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.