Evidence mapPaperPMID 24633153Full record

ArticleCellular and molecular life sciences : CMLS2014

Redox regulation of endothelial cell fate.

Ping Song, Ming-Hui Zou

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. The Protecting Activity of RIPACUTLife (Basel, Switzerland) · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. The Procoagulant Activity of EmoxilaneLife (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Cardiac Cell Senescence and Redox Signaling.Frontiers in cardiovascular medicine · 2017
    Review
  20. 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

2 authors at 1 institution in 1 country.

Ping SongSection of Molecular Medicine, Department of Internal Medicine, University of Oklahoma Health Sciences Center, 941 Stanton L Young Blvd., Oklahoma City, OK, 73104, USA, ping-song@ouhsc.edu.
Ming-Hui Zou
University of Oklahoma Health Sciences Center · US

Funding

Reactive nitrogen species &accelerated atherosclerosisR01HL079584 · UNIVERSITY OF TENNESSEE KNOXVILLE · 2004 to 2005
$777k
Oxidant stress and diabetic endothelial dysfunctionR01HL074399 · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · 2005 to 2005
$366k
NHLBI NIH HHS R01 HL074399NHLBI NIH HHS R01 HL079584NHLBI NIH HHS R01 HL080499NHLBI NIH HHS R01 HL089920NHLBI NIH HHS R01 HL096032NHLBI NIH HHS R01 HL105157NHLBI NIH HHS R01 HL110488NIA NIH HHS R01 AG047776
6 · The paper itself

Abstract

Endothelial cells (ECs) are present throughout blood vessels and have variable roles in both physiological and pathological settings. EC fate is altered and regulated by several key factors in physiological or pathological conditions. Reactive nitrogen species and reactive oxygen species derived from NAD(P)H oxidases, mitochondria, or nitric oxide-producing enzymes are not only cytotoxic but also compose a signaling network in the redox system. The formation, actions, key molecular interactions, and physiological and pathological relevance of redox signals in ECs remain unclear. We review the identities, sources, and biological actions of oxidants and reductants produced during EC function or dysfunction. Further, we discuss how ECs shape key redox sensors and examine the biological functions, transcriptional responses, and post-translational modifications evoked by the redox system in ECs. We summarize recent findings regarding the mechanisms by which redox signals regulate the fate of ECs and address the outcome of altered EC fate in health and disease. Future studies will examine if the redox biology of ECs can be targeted in pathophysiological conditions.

Indexed as

Oxidation-ReductionAnimalsApoptosisCardiovascular DiseasesCell CycleCell MovementCell TransdifferentiationCysteineDiabetes MellitusEndothelial CellsForkhead Transcription FactorsHumansHydrogen SulfideInflammationModels, BiologicalNeoplasmsCysteineForkhead Transcription FactorsHydrogen SulfideNF-E2-Related Factor 2Nitric OxideOxidoreductasesReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID24633153
PMCPMC4134393
OpenAlexW2058467412

What Socratic holds

Textmetadata
LicenceTDM
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.