Evidence map›Paper›PMID 35370493›Full record

ReviewThe Yale journal of biology and medicine2022

Oxidative Stress and Inflammation in Cardiovascular Diseases and Cancer: Role of Non-coding RNAs.

Pieterjan Ginckels, Paul Holvoet

Open access · greenAbstract readReview
In one paragraph

Review in The Yale journal of biology and medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. LncRNAs as Emerging Diagnostic Biomarkers for Cardiovascular Diseases: Evidence Synthesis Through Systematic Review and Meta-Analysis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Cancer as a novel risk factor for major cardiovascular adverse events in secondary prevention.International journal of cardiology. Cardiovascular risk and prevention · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. miRNAs and T cell-mediated Immune Response in Disease.The Yale journal of biology and medicine · 2025
    Review
  15. Omics research in atherosclerosis.Molecular and cellular biochemistry · 2025
    Review
  16. Article
  17. Article
  18. The role of miR-155 in cardiovascular diseases: Potential diagnostic and therapeutic targets.International journal of cardiology. Cardiovascular risk and prevention · 2025
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Pieterjan GinckelsDepartment of Architecture, Brussels and Gent, KU Leuven, Leuven, Belgium.
Paul HolvoetExperimental Cardiology, KU Leuven, Leuven, Belgium.
KU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High oxidative stress, Th1/Th17 immune response, M1 macrophage inflammation, and cell death are associated with cardiovascular diseases. Controlled oxidative stress, Th2/Treg anti-tumor immune response, M2 macrophage inflammation, and survival are associated with cancer. MiR-21 protects against cardiovascular diseases but may induce tumor growth by retaining the anti-inflammatory M2 macrophage and Treg phenotypes and inhibiting apoptosis. Down-regulation of let-7, miR-1, miR-9, miR-16, miR-20a, miR-22a, miR-23a, miR-24a, miR-26a, miR-29, miR-30a, miR-34a, miR-124, miR-128, miR-130a, miR-133, miR-140, miR-143-145, miR-150, miR-153, miR-181a, miR-378, and miR-383 may aid cancer cells to escape from stresses. Upregulation of miR-146 and miR-223 may reduce anti-tumor immune response together with miR-21 that also protects against apoptosis. MiR-155 and silencing of let-7e, miR-125, and miR-126 increase anti-tumor immune response. MiR expression depends on oxidative stress, cytokines, MYC, and TGF-β, and expression of silencing lncRNAs and circ-RNAs. However, one lncRNA or circ-RNA may have opposite effects by targeting several miRs. For example, PVT1 induces apoptosis by targeting miR-16a and miR-30a but inhibits apoptosis by silencing miR-17. In addition, levels of a non-coding RNA in a cell type depend not only on expression in that cell type but also on an exchange of microvesicles between cell types and tumors. Although we got more insight into the function of a growing number of individual non-coding RNAs, overall, we do not know enough how several of them interact in functional networks and how their expression changes at different stages of disease progression.

Indexed as

Cardiovascular DiseasesMicroRNAsNeoplasmsRNA, Long NoncodingHumansInflammationOxidative StressMicroRNAsMirn140 microRNA, humanMIRN153 microRNA, humanMIRN383 microRNA, humanRNA, Long Noncodingatherosclerosiscancercardiomyopathyinflammationnon-coding RNAsoxidative stress

Identifiers

PMID35370493
PMCPMC8961704
OpenAlexW4226441342

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.