Evidence map›Paper›PMID 24055979›Full record

ReviewBiochimica et biophysica acta2014

Mitochondrial permeability transition pore is a potential drug target for neurodegeneration.

Valasani Koteswara Rao, Emily A Carlson, Shirley Shidu Yan

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
10.2field-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

121 citing papers in PubMed, 321 citations in OpenAlex.

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  9. Post-Operative Delirium in Elderly Patients: A Narrative Review.International journal of molecular sciences · 2025
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  17. Antiplasmodial evidence, host mitochondrial biology and possible mechanisms of action of a composite extract ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2024
    Article
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61 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Valasani Koteswara RaoDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, KS 66047, USA.
Emily A CarlsonDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, KS 66047, USA.
Shirley Shidu YanDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, KS 66047, USA. Electronic address: shidu@ku.edu.
University of Kansas · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
Role of Cyclophilin D in Abeta-induced synaptic injuryR37AG037319 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2010 to 2019
$3.1M
Structural and Functional Properties of cyclophilin D and Abeta interaction.R01GM095355 · NIGMS · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2010 to 2013
$1.5M
NIA NIH HHS P30 AG035982NIA NIH HHS R37 AG037319NIA NIH HHS R37AG037319NIGMS NIH HHS R01 GM095355NIGMS NIH HHS R01GM095355
6 · The paper itself

Abstract

Mitochondrial permeability transition pore (mPTP) plays a central role in alterations of mitochondrial structure and function leading to neuronal injury relevant to aging and neurodegenerative diseases including Alzheimer's disease (AD). mPTP putatively consists of the voltage-dependent anion channel (VDAC), the adenine nucleotide translocator (ANT) and cyclophilin D (CypD). Reactive oxygen species (ROS) increase intra-cellular calcium and enhance the formation of mPTP that leads to neuronal cell death in AD. CypD-dependent mPTP can play a crucial role in ischemia/reperfusion injury. The interaction of amyloid beta peptide (Aβ) with CypD potentiates mitochondrial and neuronal perturbation. This interaction triggers the formation of mPTP, resulting in decreased mitochondrial membrane potential, impaired mitochondrial respiration function, increased oxidative stress, release of cytochrome c, and impaired axonal mitochondrial transport. Thus, the CypD-dependent mPTP is directly linked to the cellular and synaptic perturbations observed in the pathogenesis of AD. Designing small molecules to block this interaction would lessen the effects of Aβ neurotoxicity. This review summarizes the recent progress on mPTP and its potential therapeutic target for neurodegenerative diseases including AD.

Indexed as

Molecular Targeted TherapyAnimalsCyclophilinsHumansIschemiaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreModels, BiologicalNerve DegenerationPeptidyl-Prolyl Isomerase FCyclophilinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FAlzheimer's diseaseAmyloid βCyclophilin DMitochondrial permeability transition poreNeurodegeneration

Identifiers

PMID24055979
PMCPMC3991756
OpenAlexW2159546257

What OpenQuestion holds

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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.