Evidence map›Paper›PMID 23721657›Full record

ReviewProgress in neuro-psychopharmacology & biological psychiatry2013

Dual effects of neuroprotection and neurotoxicity by general anesthetics: role of intracellular calcium homeostasis.

Huafeng Wei, Saadet Inan

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neuro-psychopharmacology & biological psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Pharmacological properties and mechanisms of Notoginsenoside R1 in ischemia-reperfusion injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2023
    Review
  5. Anesthetics and Cell-Cell Communication: Potential CaInternational journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Prevention of Injury-Induced Osteoarthritis in Rodent Temporomandibular Joint by Targeting Chondrocyte CaSR.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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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 1 institution in 1 country.

Huafeng WeiDepartment of Anesthesiology and Critical Care, University of Pennsylvania, 305 John Morgan Building, 3620 Hamilton Walk, Philadelphia, PA 19104, USA. Electronic address: weih@uphs.upenn.edu.
Saadet Inan
University of Pennsylvania · US

Funding

Mechanisms of Anesthesia Mediated NeurotoxicityR01GM084979 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI WEI, HUAFENG · 2008 to 2018
$2.8M
Volatile anesthetics, calcium homeostasis and apoptosisK08GM073224 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI WEI, HUAFENG · 2005 to 2009
$639k
NIGMS NIH HHS 1-K08-GM-073224NIGMS NIH HHS 1-R01GM084979-02NIGMS NIH HHS 3R01GM084979-02S1NIGMS NIH HHS K08 GM073224NIGMS NIH HHS R01 GM084979
6 · The paper itself

Abstract

Although general anesthetics have long been considered neuroprotective, there are growing concerns about neurotoxicity. Preclinical studies clearly demonstrated that commonly used general anesthetics are both neuroprotective and neurotoxic, with unclear mechanisms. Recent studies suggest that differential activation of inositol 1,4,5-trisphosphate receptors, a calcium release channel located on the membrane of endoplasmic reticulum (ER), play important role on determining the fate of neuroprotection or neurotoxicity by general anesthetics. General anesthetics at low concentrations for short duration are sublethal stress factors which induce endogenous neuroprotective mechanisms and provide neuroprotection via adequate activation of InsP3R and moderate calcium release from ER. On the other hand, general anesthetics at high concentrations for prolonged duration are lethal stress factors which induce neuronal damage by over activation of InsP3R and excessive and abnormal Ca(2+) release from ER. This review emphasizes the dual effects of both neuroprotection and neurotoxicity via differential regulation of intracellular Ca(2+) homeostasis by commonly used general anesthetics and recommends strategy to maximize neuroprotective but minimize neurotoxic effects of general anesthetics.

Indexed as

Anesthetics, GeneralAnimalsCalciumHomeostasisHumansNeuroprotective AgentsNeurotoxicity SyndromesAnesthetics, GeneralCalciumNeuroprotective Agents3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide5-HD5-HydroxydecanoateAktAnesthesiaAnestheticsCalciumEndoplasmic reticulumERERKExtracellular signal-regulated kinasesGABAGamma-aminobutyric acidGlycogen synthase kinase 3βGSK3βInsP(3)RInsP(3) receptorsLactate dehydrogenaseLDHlong term potentiationLTPMAPKMitochondrial permeability transition poresMitogen-activated protein kinasemPTPMTTNeurodegenerationNeuroprotectionNeurotoxicityNMDAN-methyl-D-aspartateOGDOxygen-glucose deprivationProtein kinase BRyanodine receptorsRYRsVDCCVoltage dependent Ca(2+) channelsXcXestospongin C

Identifiers

PMID23721657
PMCPMC3791176
OpenAlexW2048860552

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.