Evidence map›Paper›PMID 31557225›Full record

ArticlePloS one2019

Mitochondrial fragmentation and network architecture in degenerative diseases.

Syed I Shah, Johanna G Paine, Carlos Perez, Ghanim Ullah

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Mitochondrial heterogeneity in diseases.Signal transduction and targeted therapy · 2023
    Review
  10. Article
  11. Review
  12. Oxidation of DJ-1 Cysteines in Retinal Pigment Epithelium Function.International journal of molecular sciences · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mitoprotective Effects ofFrontiers in pharmacology · 2021
    Review
  18. 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

4 authors at 1 institution in 1 country.

Syed I ShahDepartment of Physics, University of South Florida, Tampa, FL, United States of America.
Johanna G PaineDepartment of Physics, University of South Florida, Tampa, FL, United States of America.
Carlos PerezDepartment of Physics, University of South Florida, Tampa, FL, United States of America.
Ghanim UllahDepartment of Physics, University of South Florida, Tampa, FL, United States of America.ORCID 0000-0002-3716-8742
University of South Florida · US

Funding

A multi-scale data-driven model of the Abeta pore function and Ca2+ toxicity in Alzheimer's diseaseR01AG053988 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI DEMURO, ANGELO, ULLAH, GHANIM · 2016 to 2020
$2.1M
NIA NIH HHS R01 AG053988
6 · The paper itself

Abstract

Fragmentation of mitochondrial network has been implicated in many neurodegenerative, renal, and metabolic diseases. However, a quantitative measure of the microscopic parameters resulting in the impaired balance between fission and fusion of mitochondria and consequently the fragmented networks in a wide range of pathological conditions does not exist. Here we present a comprehensive analysis of mitochondrial networks in cells with Alzheimer's disease (AD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), optic neuropathy (OPA), diabetes/cancer, acute kidney injury, Ca2+ overload, and Down Syndrome (DS) pathologies that indicates significant network fragmentation in all these conditions. Furthermore, we found key differences in the way the microscopic rates of fission and fusion are affected in different conditions. The observed fragmentation in cells with AD, HD, DS, kidney injury, Ca2+ overload, and diabetes/cancer pathologies results from the imbalance between the fission and fusion through lateral interactions, whereas that in OPA, PD, and ALS results from impaired balance between fission and fusion arising from longitudinal interactions of mitochondria. Such microscopic difference leads to major disparities in the fine structure and topology of the network that could have significant implications for the way fragmentation affects various cell functions in different diseases.

Indexed as

Mitochondrial DynamicsAnimalsCaenorhabditis elegansCell LineDisease Models, AnimalFibroblastsHumansImage Processing, Computer-AssistedIntravital MicroscopyMiceMicroscopy, FluorescenceMitochondriaNeurodegenerative DiseasesRats

Identifiers

PMID31557225
PMCPMC6762132
OpenAlexW2975999621

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.