Evidence map›Paper›PMID 25036700›Full record

ArticleThe Journal of clinical investigation2014

The cystine/glutamate antiporter: when too much of a good thing goes bad.

Kathryn J Reissner

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kathryn J Reissner
University of North Carolina at Chapel Hill · US

Funding

Contributions of Glial Glutamate Transport and Transmission to Drug AbuseR00DA031790 · NIDA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI REISSNER, KATHRYN JOANNA · 2013 to 2016
$924k
Contributions of Glial Glutamate Transport and Transmission to Drug AbuseK99DA031790 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI REISSNER, KATHRYN JOANNA · 2012 to 2013
$240k
NIDA NIH HHS DA031790NIDA NIH HHS K99 DA031790NIDA NIH HHS R00 DA031790
6 · The paper itself

Abstract

Glutamate excitotoxicity represents a major cellular component of ischemic brain injury. In this issue of the JCI, Soria and colleagues reveal that the cystine/glutamate exchanger is an important source of excitotoxic glutamate in response to ischemia induced by oxygen and glucose deprivation. As the exchanger is a primary determinant of both extracellular glutamate and intracellular glutathione, the findings from this study not only provide important insight into the mechanisms of brain ischemia but also demonstrate the complexity of the yin and yang of glutamate homeostasis and cellular redox balance.

Indexed as

Amino Acid Transport System y+AnimalsBrain IschemiaGlutamic AcidAmino Acid Transport System y+Glutamic AcidSlc7a11 protein, mouse

Identifiers

PMID25036700
PMCPMC4109541
OpenAlexW1993857443

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.