Evidence map›Paper›PMID 30081095›Full record

ReviewDrug discovery today2018

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

Komal Kalani, Shi Fang Yan, Shirley ShiDu Yan

Abstract readReview
In one paragraph

Review in Drug discovery today, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
–field-weighted citation impact
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

60 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. [Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  16. Article
  17. Article
  18. Differential CaFrontiers in synaptic neuroscience · 2025
    Article
  19. Article
  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

3 authors.

Komal KalaniDepartment of Pharmacology and Toxicology, Higuchi Bioscience Center, School of Pharmacy, University of Kansas, Lawrence, KS 66047, USA.
Shi Fang YanDepartment of Pharmacology and Toxicology, Higuchi Bioscience Center, School of Pharmacy, University of Kansas, Lawrence, KS 66047, USA.
Shirley ShiDu YanDepartment of Pharmacology and Toxicology, Higuchi Bioscience Center, School of Pharmacy, University of Kansas, Lawrence, KS 66047, USA. Electronic address: shirley.yan@ku.edu.

Funding

University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jaime Perales Puchalt · 2021 to 2026
$25.3M
University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BROOKS, WILLIAM M. · 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
Pink1, amyloid pathology, and mitochondrial quality control in Alzheimer's DiseaseRF1AG054320 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2018 to 2018
$2.8M
TOMM40-mediated mitochondrial dysfunction and Alzheimers diseaseR01AG053041 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2017 to 2021
$2.7M
Mitochondrial degrading enzyme, synaptic mitochondrial function in AD mouse modelR01AG044793 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2014 to 2018
$1.9M
RAGE and mitochondrial degeneration in diabetesR01NS089116 · NINDS · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2015 to 2018
$1.5M
PINK1 signaling and synaptic mitochondria integrity in ADR21AG058985 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHI FANG · 2018 to 2019
$417k
TOMM40-mediated mitochondrial dysfunction and Alzheimers diseaseR56AG053041 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2016 to 2016
$387k
NIA NIH HHS P30 AG035982NIA NIH HHS P30 AG072973NIA NIH HHS R01 AG044793NIA NIH HHS R01 AG053041NIA NIH HHS R21 AG058985NIA NIH HHS R37 AG037319NIA NIH HHS R56 AG053041NIA NIH HHS RF1 AG054320NINDS NIH HHS R01 NS089116
6 · The paper itself

Abstract

The mitochondrial permeability transition pore (mPTP) has been considered a key contributor to cell death, inducing the process in several major neurodegenerative diseases. To date, the molecular nature of the mPTP remains confounding but its significance is universally acknowledged. Several targets have been screened and inhibition of mPTP has emerged as an attractive field for researchers. Nowadays, in silico-directed studies help to explore new small molecules targeting the mPTP to improve their drug-like properties and bioactivity. Here, we briefly summarize the role of mPTP in neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson disease (PD), and Huntington's disease (HD), and discusses current and future potential therapeutic targets.

Indexed as

AnimalsCell DeathHumansMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNeurodegenerative DiseasesSmall Molecule LibrariesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreSmall Molecule Libraries

Identifiers

PMID30081095
PMCPMC6449145

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.