Evidence map›Paper›PMID 29986211›Full record

ArticleRedox biology2018

MicroRNAs mediate the senescence-associated decline of NRF2 in endothelial cells.

Suvi M Kuosmanen, Virve Sihvola, Emilia Kansanen, Minna U Kaikkonen, Anna-Liisa Levonen

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The KEAP1-NRF2 System in Healthy Aging and Longevity.Antioxidants (Basel, Switzerland) · 2021
    Review
  16. Article
  17. Article
  18. Vascular Stress Signaling in Hypertension.Circulation research · 2021
    Review
  19. Article
  20. Aging and Protein Kinases.Advances in experimental medicine and biology · 2021
    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

5 authors at 1 institution in 1 country.

Suvi M KuosmanenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Virve SihvolaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Emilia KansanenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Minna U KaikkonenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Anna-Liisa LevonenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland. Electronic address: anna-liisa.levonen@uef.fi.
University of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress predisposes to several aging-associated diseases, such as cardiovascular diseases and cancer. In aging, increase in the production of reactive oxygen species is typically accompanied with a decline in adaptive stress responses to oxidative stress. The decline is primarily due to a decrease in antioxidant production. Nuclear factor E2-Related Factor 2 (NRF2) is a key transcription factor regulating oxidative and electrophilic stress responses, but it has also been shown to play a role in the regulation of cell metabolism. NRF2 expression declines in aging, but the mechanisms remain unclear. In this study, we show that microRNAs (miRNAs) that are abundant in old endothelial cells decrease NRF2 expression by direct targeting of NRF2 mRNA. The effect is reversed by miRNA inhibition. The senescence-associated downregulation of NRF2 decreases endothelial glycolytic activity and stress tolerance both of which are restored after reinstating NRF2. Manipulation of the senescence-associated miRNA levels affects the glycolytic activity and stress tolerance consistently with the NRF2 results. We conclude that senescence-associated miRNAs are involved in the decline of NRF2 expression, thus contributing to the repression of adaptive responses during cell senescence.

Indexed as

Cellular SenescenceCell ProliferationDown-RegulationEndothelial CellsGene Expression RegulationGlycolysisHumansHuman Umbilical Vein Endothelial CellsMicroRNAsNF-E2-Related Factor 2Oxidative StressMicroRNAsNFE2L2 protein, humanNF-E2-Related Factor 2AgingEndothelial cellMicroRNANRF2Senescence

Identifiers

PMID29986211
PMCPMC6037909
OpenAlexW2809433329

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.