Evidence map›Paper›PMID 20635093›Full record

ReviewPflugers Archiv : European journal of physiology2010

Obesity and aging: determinants of endothelial cell dysfunction and atherosclerosis.

Matthias Barton

Open access · bronzeAbstract 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 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of obesity in chronic kidney disease progression.Current research in physiology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Restricted Intimal CaFrontiers in physiology · 2022
    Article
  10. Article
  11. Article
  12. The aging endothelium.Vascular biology (Bristol, England) · 2021
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Effect of rosuvastatin on the expression of candidate geneExperimental and therapeutic medicine · 2018
    Article
  19. Article
  20. Vascular structural and functional changes: their association with causality in hypertension: models, remodeling and relevance.Hypertension research : official journal of the Japanese Society of Hypertension · 2017
    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

1 author at 1 institution in 1 country.

Matthias BartonMolecular Internal Medicine, University of Zurich, LTK Y44 G22, Winterthurerstrasse 190, CH-8057, Zürich, Switzerland. barton@access.uzh.ch
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells are both the source and target of factors contributing to atherosclerosis. After the discovery of the endothelium-derived relaxing factor (EDRF) by Robert F. Furchgott in 1980 it soon became clear that endothelial cells also release vasoactive factors distinct from nitric oxide (NO) namely, endothelium-derived contracting factors (EDCF) as well as hyperpolarizing factors (EDHF). Vasoactive factors derived from endothelial cells include NO/EDRF, reactive oxygen species, endothelins and angiotensins which have either EDRF or EDCF functions, cyclooxygenase-derived EDCFs and EDRFs, and EDHFs. Endothelial factors are formed by enzymes such as NO synthase, cyclooxygenase, converting enyzmes, NADPH oxidases, and epoxigenases, among others, and participate in the regulation of vascular homeostasis under physiological conditions; however, their abnormal regulation due to endothelial cell dysfunction contributes to disease processes such as atherosclerosis, arterial hypertension, and renal disease. Because of recent changes in world demographics and the declining health status of the world's population, both aging and obesity as independent risk factors for atherosclerosis-related diseases such as coronary artery disease and stroke, will continue to increase in the years to come. Obesity and associated conditions such as arterial hypertension and diabetes are now also some of the primary health concerns among children and adolescents. The similarities of pathomechanisms activated in obesity and aging suggest that obesity--at least in the vasculature--can be considered to have effects consistent with accelerated, "premature" aging. Pathomechanisms as well as the clinical issues of obesity- and aging-associated vascular changes important for atherosclerosis development and prevention are discussed.

Indexed as

AdolescentAgingAngiotensinsAnimalsAtherosclerosisChildEndothelinsEndothelium, VascularHumansInflammationMiceNitric OxideObesityOxidative StressVascular DiseasesVasoconstrictor AgentsAngiotensinsEndothelinsNitric OxideVasoconstrictor AgentsVasodilator Agents

Identifiers

PMID20635093
OpenAlexW2048975480

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.