Evidence map›Paper›PMID 34076811›Full record

ArticleInflammation2021

MicroRNA-181b Inhibits Inflammatory Response and Reduces Myocardial Injury in Sepsis by Downregulating HMGB1.

Lan Ling, Lida Zhi, Haifeng Wang, Yihuan Deng, Chengdong Gu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. miR-181b regulates vascular endothelial aging by modulating an MAP3K3 signaling pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. High Mobility Group Proteins in Sepsis.Frontiers in immunology · 2022
    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

5 authors at 1 institution in 1 country.

Lan Ling *Emergency Department, China-Japan Friendship Hospital, No. 2, Yinghua East Street, Chaoyang District, Beijing, 100029, People's Republic of China.
Lida ZhiEmergency Department, China-Japan Friendship Hospital, No. 2, Yinghua East Street, Chaoyang District, Beijing, 100029, People's Republic of China.
Haifeng Wang *Department of Nephropathy, China-Japan Friendship Hospital, Beijing, 100029, People's Republic of China.
Yihuan DengEmergency Department, China-Japan Friendship Hospital, No. 2, Yinghua East Street, Chaoyang District, Beijing, 100029, People's Republic of China.
Chengdong GuEmergency Department, China-Japan Friendship Hospital, No. 2, Yinghua East Street, Chaoyang District, Beijing, 100029, People's Republic of China. gguchengdong@126.com.
China-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are short endogenous noncoding RNAs regulating protein translation. However, the specific mechanism by which miR-181b influences sepsis via high-mobility group box-1 protein (HMGB1) still remains unknown. Thus, the aim of this study is to investigate the mechanism of miR-181b in regulating inflammatory response in sepsis-induced myocardial injury through targeting high-mobility group box-1 protein (HMGB1). Through cecal ligation and puncture (CLP), the rat model of sepsis was established. Then, the effect of altered expression of miR-181b and HMGB1 on cardiomyocytes was investigated. The positive expression rate of HMGB1, concentration of inflammatory factors, and serum myocardial enzyme of myocardial tissues were determined. Besides, the binding site between miR-181b and HMGB1 was determined by bioinformatics information and dual-luciferase reporter gene assay. The expression of related genes in cells of each group was determined by RT-qPCR and western blot analysis, and the apoptosis rate of transfected cells in each group was determined by TUNEL assay. HMGB1 expression and inflammatory factors were significantly increased in myocardial tissue of rats with sepsis. Cell morphology and the infiltration of inflammatory cells were significantly improved by overexpression of miR-181b. miR-181b directly targeted HMGB1, and downregulation of HMGB1 reduced inflammatory factors and myocardial injury and inhibited cardiomyocyte apoptosis in sepsis. This present study suggests that miR-181b decreased inflammatory factors and reduced myocardial injury in sepsis through downregulation of HMGB1. Thus, a better understanding of this process may aid in the development of novel therapeutic agents in sepsis.

Indexed as

AnimalsDown-RegulationHMGB1 ProteinInflammation MediatorsMaleMicroRNAsMyocardial IschemiaMyocardiumMyocytes, CardiacRatsRats, Sprague-DawleySepsisHbp1 protein, ratHMGB1 ProteinInflammation MediatorsMicroRNAsMIRN181 microRNA, ratapoptosisHMGB1inflammatory responsemicroRNA-181bmyocardial injurysepsis

Identifiers

PMID34076811
OpenAlexW3164419274

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.