Evidence map›Paper›PMID 21248240›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Carbon monoxide protects against oxidant-induced apoptosis via inhibition of Kv2.1.

Mark L Dallas, John P Boyle, Carol J Milligan, Rachael Sayer, Talitha L Kerrigan, Connor McKinstry, Peiyuan Lu, Jamel Mankouri, Mark Harris, Jason L Scragg and 2 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Carbon monoxide activation of delayed rectifier potassium currents of human cardiac fibroblasts through diverse pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Article
  7. Article
  8. Article
  9. Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020
    Review
  10. Article
  11. Gas Signaling Molecules and Mitochondrial Potassium Channels.International journal of molecular sciences · 2018
    Review
  12. Carbon monoxide in lung cell physiology and disease.American journal of physiology. Cell physiology · 2018
    Review
  13. Review
  14. Article
  15. Review
  16. Gasotransmitter Heterocellular Signaling.Antioxidants & redox signaling · 2017
    Article
  17. Review
  18. Article
  19. Functional Interactions between BKOxidative medicine and cellular longevity · 2016
    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

12 authors at 2 institutions in 2 countries.

Mark L DallasDivision of Cardiovascular and Neuronal Remodelling, Faculty of Medicine and Health, University of Leeds, Leeds, UK.
John P Boyle
Carol J Milligan
Rachael Sayer
Talitha L Kerrigan
Connor McKinstry
Peiyuan Lu
Jamel Mankouri
Mark Harris
Jason L Scragg
Hugh A Pearson
Chris Peers
University of Leeds · GBHebei General Hospital · CN

Funding

British Heart Foundation PG/09/013/26885Medical Research Council G0600936Wellcome Trust 096670
6 · The paper itself

Abstract

Oxidative stress induces neuronal apoptosis and is implicated in cerebral ischemia, head trauma, and age-related neurodegenerative diseases. An early step in this process is the loss of intracellular K(+) via K(+) channels, and evidence indicates that K(v)2.1 is of particular importance in this regard, being rapidly inserted into the plasma membrane in response to apoptotic stimuli. An additional feature of neuronal oxidative stress is the up-regulation of the inducible enzyme heme oxygenase-1 (HO-1), which catabolizes heme to generate biliverdin, Fe(2+), and carbon monoxide (CO). CO provides neuronal protection against stresses such as stroke and excitotoxicity, although the underlying mechanisms are not yet elucidated. Here, we demonstrate that CO reversibly inhibits K(v)2.1. Channel inhibition by CO involves reactive oxygen species and protein kinase G activity. Overexpression of K(v)2.1 in HEK293 cells increases their vulnerability to oxidant-induced apoptosis, and this is reversed by CO. In hippocampal neurons, CO selectively inhibits K(v)2.1, reverses the dramatic oxidant-induced increase in K(+) current density, and provides marked protection against oxidant-induced apoptosis. Our results provide a novel mechanism to account for the neuroprotective effects of CO against oxidative apoptosis, which has potential for therapeutic exploitation to provide neuronal protection in situations of oxidative stress.

Indexed as

2,2'-DipyridylAnimalsApoptosisCarbon MonoxideCaspase 3Caspase 7Cell LineDisulfidesElectrophysiologyHEK293 CellsHumansImmunohistochemistryIn Situ Nick-End LabelingOxidantsRatsRats, Wistar2,2'-Dipyridyl2,2'-dipyridyl disulfideCarbon MonoxideCaspase 3Caspase 7DisulfidesOxidantsShab Potassium Channels

Identifiers

PMID21248240
PMCPMC7615704
OpenAlexW2126176177

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.