Evidence map›Paper›PMID 34926662›Full record

ArticleAnnals of translational medicine2021

miR-155 regulates pro- and anti-inflammatory cytokine expression in human monocytes during chronic hepatitis C virus infection.

Yun Zhou, Peixin Zhang, Xuyang Zheng, Chuantao Ye, Mengyuan Li, Peiyu Bian, Chao Fan, Ying Zhang

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Novel Tryptanthrin Derivatives with Selectivity asMolecules (Basel, Switzerland) · 2023
    Article
  2. Review
  3. Article
  4. Article
  5. Inhibition of miR-155 Attenuates CD14Clinical, cosmetic and investigational dermatology · 2022
    Article
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

8 authors at 1 institution in 1 country.

Yun Zhou *Department of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Peixin Zhang *Department of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Xuyang ZhengDepartment of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Chuantao YeDepartment of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Mengyuan LiDepartment of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Peiyu BianDepartment of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Chao FanDepartment of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Ying ZhangDepartment of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatitis C virus (HCV) dysregulates innate and adaptive immune responses while monocytes (M) play a crucial role in linking innate and adaptive immunity to control viral infection. A transcription factor T-bet is upregulated to dampen M functions via the c-Jun N-terminal kinase (JNK) pathway, followed by enhanced Tim-3 expression in chronic HCV infection. However, the molecular mechanisms that control the expression in M are yet unknown. miR-155 has been implicated as a key regulator controlling diverse biological processes through posttranscriptional repression, but the influences of miR-155 on these regulators and effectors still need to be studied.

methodsForty HCV-infected patients and 40 healthy subjects (HS) were recruited, THP-1 cells (human acute monocyte leukemia cell line) were cultured with HCV-infected Huh 7.5 cells. The expression levels of miR-155 and

resultsThe study showed that miR-155 was upregulated in CD14

conclusionsThe obtained results indicated that miR-155 upregulation in M during HCV infection enhances the activation of TNF-α and JNK pathways, promotes the expression of transcription factor T-bet, and triggers pro- and anti-inflammatory mediators. Together, these data reveal new information regarding the mechanisms of chronic HCV infection.

Indexed as

Hepatitis C virus (HCV)immune regulationmicroRNA-155 (miR-155)monocyte (M)T-bet

Identifiers

PMID34926662
PMCPMC8640902
OpenAlexW3199383344

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.