Evidence map›Paper›PMID 38607087›Full record

ReviewCells2024

Mitochondrial Permeability Transition, Cell Death and Neurodegeneration.

Artyom Y Baev, Andrey Y Vinokurov, Elena V Potapova, Andrey V Dunaev, Plamena R Angelova, Andrey Y Abramov

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  3. Review
  4. The role of mitochondrial Na⁺/Ca²⁺ exchanger in brain cell aging.Journal of bioenergetics and biomembranes · 2026
    Review
  5. Article
  6. Caffeic Acid Protects Keratinocytes from PMBiomolecules & therapeutics · 2026
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. AMarine drugs · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Mechanistic Insights into the Neuroprotective Potential ofPharmaceuticals (Basel, Switzerland) · 2025
    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

6 authors at 3 institutions in 3 countries.

Artyom Y BaevLaboratory of Experimental Biophysics, Centre for Advanced Technologies, Tashkent 100174, Uzbekistan.ORCID 0000-0003-1582-5059
Andrey Y VinokurovCell Physiology and Pathology Laboratory, Orel State University, Orel 302026, Russia.ORCID 0000-0001-8436-1353
Elena V PotapovaCell Physiology and Pathology Laboratory, Orel State University, Orel 302026, Russia.ORCID 0000-0002-9227-6308
Andrey V DunaevCell Physiology and Pathology Laboratory, Orel State University, Orel 302026, Russia.ORCID 0000-0003-4431-6288
Plamena R AngelovaDepartment of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK.ORCID 0000-0003-4596-9117
Andrey Y AbramovDepartment of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK.ORCID 0000-0002-7646-7235
Orel State University named after I.S. Turgenev · RUNational Hospital for Neurology and Neurosurgery · GBNational University of Uzbekistan · UZ

Funding

Russian Science Foundation 22-15-00317
6 · The paper itself

Abstract

Neurodegenerative diseases are chronic conditions occurring when neurons die in specific brain regions that lead to loss of movement or cognitive functions. Despite the progress in understanding the mechanisms of this pathology, currently no cure exists to treat these types of diseases: for some of them the only help is alleviating the associated symptoms. Mitochondrial dysfunction has been shown to be involved in the pathogenesis of most the neurodegenerative disorders. The fast and transient permeability of mitochondria (the mitochondrial permeability transition, mPT) has been shown to be an initial step in the mechanism of apoptotic and necrotic cell death, which acts as a regulator of tissue regeneration for postmitotic neurons as it leads to the irreparable loss of cells and cell function. In this study, we review the role of the mitochondrial permeability transition in neuronal death in major neurodegenerative diseases, covering the inductors of mPTP opening in neurons, including the major ones-free radicals and calcium-and we discuss perspectives and difficulties in the development of a neuroprotective strategy based on the inhibition of mPTP in neurodegenerative disorders.

Indexed as

Mitochondrial Transmembrane Permeability-Driven NecrosisNeurodegenerative DiseasesCell DeathHumansMitochondriaNecrosisastrocytecell deathmitochondrial permeability transitionneurodegenerationneuron

Identifiers

PMID38607087
PMCPMC11011324
OpenAlexW4394580612

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.