Evidence map›Paper›PMID 35626707›Full record

ReviewCells2022

The Role of MiR-181 Family Members in Endothelial Cell Dysfunction and Tumor Angiogenesis.

Chun Yang, Victor Passos Gibson, Pierre Hardy

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
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  6. Review
  7. Review
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  9. CouldBiomedicines · 2025
    Article
  10. Review
  11. Review
  12. Expert opinion on therapeutic targets · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
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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 1 country.

Chun YangResearch Center of CHU Sainte-Justine, University of Montréal, Quebec, QC H3T 1C5, Canada.
Victor Passos GibsonDepartments of Pharmacology and Physiology, University of Montréal, Quebec, QC H3T 1C5, Canada.
Pierre HardyResearch Center of CHU Sainte-Justine, University of Montréal, Quebec, QC H3T 1C5, Canada.ORCID 0000-0002-9846-7113
Centre Hospitalier Universitaire Sainte-Justine · CAUniversité de Montréal · CA

Funding

CIHR 426236
6 · The paper itself

Abstract

Endothelial dysfunction plays a critical role in many human angiogenesis-related diseases, including cancer and retinopathies. Small non-coding microRNAs (miRNAs) repress gene expression at the post-transcriptional level. They are critical for endothelial cell gene expression and function and are involved in many pathophysiological processes. The miR-181 family is one of the essential angiogenic regulators. This review summarizes the current state of knowledge of the role of miR-181 family members in endothelial cell dysfunction, with emphasis on their pathophysiological roles in aberrant angiogenesis. The actions of miR-181 members are summarized concerning their targets and associated major angiogenic signaling pathways in a cancer-specific context. Elucidating the underlying functional mechanisms of miR-181 family members that are dysregulated in endothelial cells or cancer cells is invaluable for developing miRNA-based therapeutics for angiogenesis-related diseases such as retinopathies, angiogenic tumors, and cancer. Finally, potential clinical applications of miR-181 family members in anti-angiogenic tumor therapy are discussed.

Indexed as

MicroRNAsVascular DiseasesEndothelial CellsHumansNeovascularization, PathologicSignal TransductionMicroRNAsMIrn181 microRNA, humanangiogenesisanti-angiogenic therapyBBB/BTBendothelial dysfunctionmiR-181nanoparticlestumor angiogenesis

Identifiers

PMID35626707
PMCPMC9140109
OpenAlexW4280549665

What Socratic holds

Textmetadata
LicenceCC BY
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.