Evidence map›Paper›PMID 25194713›Full record

ReviewCellular and molecular neurobiology2015

Mechanisms involved in the ischemic tolerance in brain: effect of the homocysteine.

Jan Lehotsky, Martin Petras, Maria Kovalska, Barbara Tothova, Anna Drgova, Peter Kaplan

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2015. 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
3.8field-weighted citation impact, top 7% 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, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Betaine-homocysteineFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Serum folate and cobalamin levels and urinary dimethylarsinic acid in US children and adults.Environmental science and pollution research international · 2018
    Article
  18. Article
  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

6 authors at 1 institution in 1 country.

Jan LehotskyJessenius Faculty of Medicine, Institute of Medical Biochemistry, Comenius University, Mala Hora 4, 036 01, Martin, Slovakia, lehotsky@jfmed.uniba.sk.
Martin Petras
Maria Kovalska
Barbara Tothova
Anna Drgova
Peter Kaplan
Comenius University Bratislava · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia (hHCy) is recognized as a co-morbid risk factor of human stroke. It also aggravates the ischemia-induced injury by increased production of reactive oxygen species, and by the homocysteinylation and thiolation of functional proteins. Ischemic preconditioning represents adaptation of the CNS to sub-lethal ischemia, resulting in increased brain tolerance to subsequent ischemia. We present here an overview of recent data on the homocysteine (Hcy) metabolism and on the genetic and metabolic causes of hHCy-related neuropathologies in humans. In this context, the review documents for an increased oxidative stress and for the functional modifications of enzymes involved in the redox balance in experimentally induced hHCy. Hcy metabolism leads also to the redox imbalance and increased oxidative stress resulting in elevated lipoperoxidation and protein oxidation, the products known to be included in the neuronal degeneration. Additionally, we examine the effect of the experimental hHCy in combination with ischemic insult, and/or with the preischemic challenge on the extent of neuronal degeneration as well as the intracellular signaling and the regulation of DNA methylation. The review also highlights that identification of the effects of co-morbid factors in the mechanisms of ischemic tolerance mechanisms would lead to improved therapeutics, especially the brain tissue.

Indexed as

AnimalsBrainBrain IschemiaHomocysteineHumansHyperhomocysteinemiaIschemic PreconditioningHomocysteine

Identifiers

PMID25194713
PMCPMC11488051
OpenAlexW2067761000

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.