Evidence map›Paper›PMID 20107832›Full record

ReviewPflugers Archiv : European journal of physiology2010

Human endothelial dysfunction: EDCFs.

Agostino Virdis, Lorenzo Ghiadoni, Stefano Taddei

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. CaInternational journal of molecular sciences · 2024
    Review
  3. Review
  4. Review
  5. CRISPR-Based Activation of Endogenous Expression ofFrontiers in cell and developmental biology · 2021
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. The COP9 signalosome and vascular function: intriguing possibilities?American journal of cardiovascular disease · 2015
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Protecting against vascular disease in brain.American journal of physiology. Heart and circulatory physiology · 2011
    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

3 authors at 1 institution in 1 country.

Agostino VirdisDepartment of Internal Medicine, University of Pisa, Via Roma, 67, 56100, Pisa, Italy.
Lorenzo Ghiadoni
Stefano Taddei
University of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human studies, conducted in the presence of clinical conditions characterized by endothelial dysfunction, evidenced that endothelial cells, in response to different agonists and physical stimuli, become a source of endothelium-derived contracting factors (EDCFs), mainly cyclooxygenase (COX)-derived prostanoids. Their production has been documented in several human diseases, mostly in essential hypertension and aging. The EDCF production was at first identified as responsible for impaired endothelium-dependent vasodilation in the forearm microcirculation of patients with essential hypertension. Subsequent studies demonstrated that COX-dependent EDCF products are also a characteristic of the aging process, and essential hypertension seems to only anticipate the phenomenon. Of note, in aging and hypertension, both indomethacin, a COX inhibitor, and vitamin C, an antioxidant, totally reverse the blunted vasodilation to acetylcholine by restoring NO availability, thus suggesting that EDCFs could be one of the major sources of oxygen free radicals. The presence of EDCFs was documented also in other clinical setting, such as coronary artery disease and estrogen deprivation. In conclusion, many human pathological conditions characterized by a decline in endothelial function are associated with a progressive decrease in NO bioavailability and increase in the production of EDCFs. The mechanisms that regulate the balance between NO and EDCFs and the processes transforming the endothelium from a protective organ to a source of vasoconstrictor, proaggregatory and promitogenic mediators, remain to be determined.

Indexed as

VasoconstrictionAgingAnimalsEndothelin-1Endothelium, VascularEstrogensForearmHumansHypertensionIndomethacinMuscle, Smooth, VascularProstaglandin-Endoperoxide SynthasesProstaglandinsReactive Oxygen SpeciesReceptor, Endothelin AReceptor, Endothelin BEndothelin-1EstrogensIndomethacinProstaglandin-Endoperoxide SynthasesProstaglandinsReactive Oxygen SpeciesReceptor, Endothelin AReceptor, Endothelin BVasoconstrictor Agents

Identifiers

PMID20107832
OpenAlexW2083396130

What OpenQuestion 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 OpenQuestion graph.