Evidence map›Paper›PMID 21540287›Full record

ArticleEndocrinology2011

Estrogen protection in Friedreich's ataxia skin fibroblasts.

Timothy E Richardson, Shao-Hua Yang, Yi Wen, James W Simpkins

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Oxidative stress in inherited mitochondrial diseases.Free radical biology & medicine · 2015
    Review
  11. Article
  12. Non-feminizing estrogens: a novel neuroprotective therapy.Molecular and cellular endocrinology · 2014
    Review
  13. Article
  14. Review
  15. Article
  16. Estrogens and aging skin.Dermato-endocrinology · 2013
    Review
  17. Review
  18. Friedreich's ataxia, frataxin, PIP5K1B: echo of a distant fracas.Oxidative medicine and cellular longevity · 2013
    Review
  19. Article
  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

4 authors at 2 institutions in 1 country.

Timothy E RichardsonInstitute for Aging and Alzheimer’s Disease Research, Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA. james.simpkins@unthsc.edu
Shao-Hua Yang
Yi Wen
James W Simpkins
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

Protein Targets of Oxidative Brain AgingP01AG022550 · NIA · WEST VIRGINIA UNIVERSITY · PI SIMPKINS, JAMES W. · 2003 to 2013
$15.7M
ROLE OF MITHOCHONDRIAL ERB IN NEURONAL VULNDERABILITY TO NEUROTOXIC STRESSP01AG027956 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SINGH, MEHARVAN · 2007 to 2017
$11.3M
NIA NIH HHS P01 AG022550NIA NIH HHS P01 AG027956NIA NIH HHS P01 AG100485NIA NIH HHS P01 AG22550
6 · The paper itself

Abstract

Estrogens have been shown to have protective effects on a wide range of cell types and animal models for many neurodegenerative diseases. The present study demonstrates the cytoprotective effects of 17β-estradiol (E2) and estrogen-like compounds in an in vitro model of Friedreich's ataxia (FRDA) using human donor FRDA skin fibroblasts. FRDA fibroblasts are extremely sensitive to free radical damage and oxidative stress, produced here using l-buthionine (S,R)-sulfoximine to inhibit de novo glutathione synthesis. We have shown that the protective effect of E2 in the face of l-buthionine (S,R)-sulfoximine -induced oxidative stress is independent of estrogen receptor-α, estrogen receptor-β or G protein-coupled receptor 30 as shown by the inability of either ICI 182,780 or G15 to inhibit the E2-mediated protection. These cytoprotective effects appear to be dependent on antioxidant properties and the phenolic structure of estradiol as demonstrated by the observation that all phenolic compounds tested were protective, whereas all nonphenolic compounds were inactive, and the observation that the phenolic compounds reduced the levels of reactive oxygen species, whereas the nonphenolic compounds did not. These data show for the first time that phenolic E2-like compounds are potent protectors against oxidative stress-induced cell death in FRDA fibroblasts and are possible candidate drugs for the treatment and prevention of FRDA symptoms.

Indexed as

AdultAntioxidantsButhionine SulfoximineCells, CulturedCell SurvivalEstradiolEstrogen Receptor ModulatorsEstrogensFibroblastsFriedreich AtaxiaGlutathioneHumansMaleNeuroprotective AgentsOxidative StressPhenolsAntioxidantsButhionine SulfoximineEstradiolEstrogen Receptor ModulatorsEstrogensGlutathioneGPER1 protein, humanNeuroprotective AgentsPhenolsReactive Oxygen SpeciesReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID21540287
PMCPMC3115615
OpenAlexW2111360430

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.