Evidence map›Paper›PMID 24323190›Full record

ReviewTranslational stroke research2013

Epigenetics and the environment: in search of the "toleroasome" vital to execution of ischemic preconditioning.

David Brand, Rajiv R Ratan

Abstract readReview
In one paragraph

Review in Translational stroke research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Epigenetics and nutritional environmental signals.Integrative and comparative biology · 2014
    Review
  9. Article
  10. SIRT1 regulation modulates stroke outcome.Translational stroke research · 2013
    Review
  11. 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 2 institutions in 1 country.

David BrandAmherst College, Amherst, MA, USA.
Rajiv R Ratan
Amherst College · USBurke Medical Research Institute · US

Funding

TRANSCRIPTIONAL RESPONSES TO MITOCHONDRIAL DYSFUNCTIONP01AG014930 · NIA · WINIFRED MASTERSON BURKE MED RES INST · PI GIBSON, GARY E · 1999 to 2020
$30.7M
NIA NIH HHS P01 AG014930NIA NIH HHS P01 AG14930-10
6 · The paper itself

Abstract

Activation and repression of gene expression are key features of ischemic tolerance. Converging lines of inquiry from several groups suggests that epigenetic proteins may transduce sublethal stresses, including bioenergetic or oxidative stress into durable (2-3 days) changes in gene expression that mediate ischemic tolerance. Here we discuss the potential mechanisms by which changes in cell state (e.g., ATP, NAD+, and oxygen) can modify specific targets including polycomb complexes, jumonji domain histone demethylases, and zinc and NAD-dependent histone decetylases and thus trigger an adaptive program. A major unanswered question is whether these proteins work in parallel or convergently as part of a "tolerosome" (tolero is the Latin word for tolerance), a multiprotein complex recruited to promoters or enhancers of specific genes, to mediate preconditioning. Whatever the case may be, epigenetic proteins are fertile targets for the treatment of stroke.

Indexed as

Epigenesis, GeneticIschemic PreconditioningBrainBrain IschemiaHistone DemethylasesHumansJumonji Domain-Containing Histone DemethylasesPolycomb-Group ProteinsHistone DemethylasesJumonji Domain-Containing Histone DemethylasesPolycomb-Group Proteins

Identifiers

PMID24323190
PMCPMC4040454
OpenAlexW1994147703

What OpenQuestion 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 OpenQuestion graph.