Evidence map›Paper›PMID 32700093›Full record

ReviewCellular and molecular neurobiology2021

Building a Bridge Between NMDAR-Mediated Excitotoxicity and Mitochondrial Dysfunction in Chronic and Acute Diseases.

Rodrigo G Mira, Waldo Cerpa

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.1field-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

51 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
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  8. Article
  9. Article
  10. Review
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  12. Review
  13. Neuronal Deletion ofBiomolecules · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Oxidative Stress in Brain Function.Antioxidants (Basel, Switzerland) · 2025
    Review
  18. Article
  19. Article
  20. Review
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.

Rodrigo G MiraLaboratorio de función y patología Neuronal, Centro de Envejecimiento y Regeneración (CARE), Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
Waldo CerpaLaboratorio de función y patología Neuronal, Centro de Envejecimiento y Regeneración (CARE), Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile. wcerpa@bio.puc.cl.ORCID http://orcid.org/0000-0001-7344-0144
Pontificia Universidad Católica de Chile · CL

Funding

Center for Excellence in Science and Technology (AFB 170005, PFB 12/2007)conicyt pre-doctoral fellowshipFondo Nacional de Desarrollo Científico y Tecnológico FONDECYT 1190620Sociedad Química y Minera de Chile (SQM) special grant "The role of lithium in human health and disease
6 · The paper itself

Abstract

Glutamate is the major excitatory neurotransmitter in the brain, and it is widely accepted to play a role in synaptic plasticity and excitotoxic cell death. Glutamate binds to several receptors, including ionotropic N-methyl-D-Aspartate receptor (NMDAR), which is essential in synaptic plasticity and excitotoxicity. This receptor is a calcium channel that is located in synaptic and extrasynaptic sites, triggering different signalling cascades in each case. The calcium entry through extrasynaptic NMDARs is linked to calcium overload in the mitochondria in neurons in vitro. The mitochondria, besides their role in ATP production in the cell, participate in calcium homeostasis, acting as a buffering organelle. Disruption of mitochondrial calcium homeostasis has been linked to neuronal death either by triggering apoptosis or driven by the opening of the mitochondrial transition pore. These cell-death mechanisms contribute to the pathophysiology of diverse diseases such as neurodegenerative Alzheimer's disease or Parkinson's disease, and acute neuropathological conditions such as stroke or traumatic brain injury. In this review, we will address the available evidence that positions the mitochondria as an essential organelle in the control of calcium-mediated toxicity, highlighting its role from the perspective of specific NMDAR signalling microdomains at the level of the central synapse.

Indexed as

AnimalsGlutamic AcidHippocampusHumansMitochondriaNeuronsReceptors, N-Methyl-D-AspartateSynapsesGlutamic AcidReceptors, N-Methyl-D-AspartateCalciumExcitotoxicityMitochondriaNMDAR

Identifiers

PMID32700093
PMCPMC11448584
OpenAlexW3044559658

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.