Evidence map›Paper›PMID 24575045›Full record

ReviewFrontiers in physiology2014

Molecular pathways of pannexin1-mediated neurotoxicity.

Valery I Shestopalov, Vladlen Z Slepak

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The Alteration Profiles of mFrontiers in neuroscience · 2022
    Article
  9. Review
  10. Review
  11. Review
  12. Functional Coupling between the P2XInternational journal of molecular sciences · 2021
    Article
  13. Review
  14. Insights into Potential Targets for Therapeutic Intervention in Epilepsy.International journal of molecular sciences · 2020
    Review
  15. Pannexin-1 Deficiency Decreases Epileptic Activity in Mice.International journal of molecular sciences · 2020
    Article
  16. Article
  17. Article
  18. The Neuroglial Dialog Between Cannabinoids and Hemichannels.Frontiers in molecular neuroscience · 2018
    Article
  19. Review
  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

2 authors at 1 institution in 2 countries.

Valery I ShestopalovDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine Miami, FL, USA ; Department of Cell Biology and Anatomy, University of Miami Miller School of Medicine Miami, FL, USA ; Vavilov Institute of General Genetics, Moscow, Russian Federation, University of Miami Miller School of Medicine Miami, FL, USA.
Vladlen Z SlepakDepartment of Molecular Pharmacology, University of Miami Miller School of Medicine Miami, FL, USA ; Neuroscience Program, University of Miami Miller School of Medicine Miami, FL, USA.
University of Miami · US

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Dmitry V Ivanov · 2004 to 2026
$12.2M
Interaction of RGS Protein with G beta subunit G beta 5.R01GM060019 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SLEPAK, VLADLEN Z · 1999 to 2013
$3.8M
The Role of Pannexin 1 Pathway in Ocular Hypertension Injury of Retinal Ganglion CellsR01EY021517 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2012 to 2020
$3.1M
Light-dependent Transducin Movement in Retinal Rods.R01EY018666 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SLEPAK, VLADLEN Z · 2009 to 2013
$1.8M
Organization of the lens core syncytiumR01EY014232 · NEI · WASHINGTON UNIVERSITY · PI SHESTOPALOV, VALERY I · 2002 to 2008
$1.8M
NEI NIH HHS P30 EY014801NEI NIH HHS R01 EY014232NEI NIH HHS R01 EY018666NEI NIH HHS R01 EY021517NIGMS NIH HHS R01 GM060019
6 · The paper itself

Abstract

Pannexin1 (Panx1) forms non-selective membrane channels, structurally similar to gap junction hemichannels, and are permeable to ions, nucleotides, and other small molecules below 900 Da. Panx1 activity has been implicated in paracrine signaling and inflammasome regulation. Recent studies in different animal models showed that overactivation of Panx1 correlates with a selective demise of several types of neurons, including retinal ganglion cells, brain pyramidal, and enteric neurons. The list of Panx1 activators includes extracellular ATP, glutamate, high K(+), Zn(2+), fibroblast growth factors (FGFs),pro-inflammatory cytokines, and elevation of intracellular Ca(2+). Most of these molecules are released following mechanical, ischemic, or inflammatory injury of the CNS, and rapidly activate the Panx1 channel. Prolonged opening of Panx1 channel induced by these "danger signals" triggers a cascade of neurotoxic events capable of killing cells. The most vulnerable cell type are neurons that express high levels of Panx1. Experimental evidence suggests that Panx1 channels mediate at least two distinct neurotoxic processes: increased permeability of the plasma membrane and activation of the inflammasome in neurons and glia. Importantly, both pharmacological and genetic inactivation of Panx1 suppresses both these processes, providing a marked protection in several disease and injury models. These findings indicate that external danger signals generated after diverse types of injuries converge to activate Panx1. In this review we discuss molecular mechanisms associated with Panx1 toxicity and the crosstalk between different pathways.

Indexed as

calciumdanger signalshemichannelinflammasomeneuronal deathneurotoxicitypannexinsignaling

Identifiers

PMID24575045
PMCPMC3920106
OpenAlexW2005263126

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.