Evidence map›Paper›PMID 38581539›Full record

ArticleMolecular neurobiology2024

Mitophagy Upregulation Occurs Early in the Neurodegenerative Process Mediated by α-Synuclein.

Sarah Hui, Jimmy George, Minesh Kapadia, Hien Chau, Zahn Bariring, Rebecca Earnshaw, Kashfia Shafiq, Lorraine V Kalia, Suneil K Kalia

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025
    Review
  9. Review
  10. 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

9 authors at 1 institution in 1 country.

Sarah HuiKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Jimmy GeorgeKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Minesh KapadiaKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Hien ChauKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Zahn BariringKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Rebecca EarnshawKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Kashfia ShafiqKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Lorraine V Kalia *Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Suneil K Kalia *Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada. suneil.kalia@utoronto.ca.ORCID http://orcid.org/0000-0003-2054-1915
University Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurogenerative movement disorder characterized by dopaminergic cell death within the substantia nigra pars compacta (SNpc) due to the aggregation-prone protein α-synuclein. Accumulation of α-synuclein is implicated in mitochondrial dysfunction and disruption of the autophagic turnover of mitochondria, or mitophagy, which is an essential quality control mechanism proposed to preserve mitochondrial fidelity in response to aging and stress. Yet, the precise relationship between α-synuclein accumulation, mitochondrial autophagy, and dopaminergic cell loss remains unresolved. Here, we determine the kinetics of α-synuclein overexpression and mitophagy using the pH-sensitive fluorescent mito-QC reporter. We find that overexpression of mutant A53T α-synuclein in either human SH-SY5Y cells or rat primary cortical neurons induces mitophagy. Moreover, the accumulation of mutant A53T α-synuclein in the SNpc of rats results in mitophagy dysregulation that precedes the onset of dopaminergic neurodegeneration. This study reveals a role for mutant A53T α-synuclein in inducing mitochondrial dysfunction, which may be an early event contributing to neurodegeneration.

Indexed as

alpha-SynucleinMitophagyUp-RegulationAnimalsCell Line, TumorDopaminergic NeuronsHumansMitochondriaMutationNerve DegenerationNeuronsRatsRats, Sprague-Dawleyalpha-SynucleinSNCA protein, humanSnca protein, ratAlpha-synucleinLysosomesMitochondria dysfunctionMitophagyNeurodegenerationParkinson’s diseaseSubstantia nigra pars compacta

Identifiers

PMID38581539
PMCPMC11496319
OpenAlexW4394012804

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.