Evidence map›Paper›PMID 39506440›Full record

ReviewCurrent molecular medicine2025

miR-144/451: A Regulatory Role in Inflammation.

Jiahao Zhu, Yanhua Feng, Lingxiao Zhang, Xialing Pang, Sheng He, Lei Fang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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

2 citing papers in PubMed.

  1. Review
  2. 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

6 authors.

Jiahao ZhuInstitute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, 225009, China.
Yanhua FengPaediatric Department, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530002, China.
Lingxiao ZhangInstitute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, 225009, China.
Xialing PangPaediatric Department, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530002, China.
Sheng HeGuangxi Key Laboratory of Reproductive Health and Birth Defects Prevention, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530002, China.
Lei FangInstitute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, 225009, China.

Funding

Opening Topic Fund of Guangxi Key Laboratory of Reproductive Health and Birth Defects Prevention GXWCH-ZDKF-2023-03
6 · The paper itself

Abstract

backgroundInflammation is the natural defense mechanism of the body in response to injury, infection, or other stimuli. Excessive or persistent inflammatory responses can lead to the development of inflammatory diseases. Therefore, elucidating the regulatory mechanisms of inflammatory cells is crucial for understanding the pathogenesis of such diseases and devising novel therapeutic approaches. Moreover, miR-144/451 plays an important role in erythroid maturity and tumour development. Herein, we have reviewed the regulatory role of miR-144/451 in inflammation.

methodsPapers on miR-144, miR-451, and inflammation were retrieved from PubMed and Web of Science to be analysed and summarised.

resultsmiR-144/451 plays a significant role in modulating inflammatory responses. Pro- and anti-inflammatory gene transcription is regulated by miR-144/451 binding to the 3' untranslated regions. Studies have shown that miR-451 inhibits the activation of various inflammatory cells, including macrophages, neutrophils, and T lymphocytes, thereby reducing the release of inflammatory mediators. However, miR-144 expression varies in different inflammatory diseases. miR-144 expression is downregulated in macrophages after induction by lipopolysaccharide, cysteine, or Mycobacterium tuberculosis, which promotes the secretion of inflammatory mediators; nonetheless, miR-144-3p overexpression in macrophages can aggravate atherosclerosis. Meanwhile, miR-144 overexpression prevents disruption of the lung endothelial cell barrier, whereas it exacerbates endothelial cell injury in Crohn's disease.

conclusionmiR-144/451 may serve as a potential target for the treatment of inflammatory diseases.

Indexed as

Gene Expression RegulationInflammationMicroRNAsAnimalsHumansMacrophagesMicroRNAsMIRN144 microRNA, humanMIRN451 microRNA, humandendritic cellendothelial cellepithelial cell.macrophagemiR-144/451neutrophilT lymphocyte

Identifiers

PMID39506440

What Socratic 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 Socratic graph.