Evidence map›Paper›PMID 29341130›Full record

ReviewJournal of neurochemistry2018

Mitochondrial function and autophagy: integrating proteotoxic, redox, and metabolic stress in Parkinson's disease.

Jianhua Zhang, Matilda Lillian Culp, Jason G Craver, Victor Darley-Usmar

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neurochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

  1. Targeting neuroinflammation in neurodegenerative disorders: the emerging potential of semaglutide.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  13. Rest and Digest-The Basal Role of Autophagy in Neurons and Its Relevance to Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2022
    Article
  14. Review
  15. Review
  16. Role of eIF5A in Mitochondrial Function.International journal of molecular sciences · 2022
    Review
  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Jianhua ZhangCenter for Free Radical Biology, Birmingham, Alabama, USA.ORCID 0000-0002-2128-9574
Matilda Lillian CulpCenter for Free Radical Biology, Birmingham, Alabama, USA.
Jason G CraverCenter for Free Radical Biology, Birmingham, Alabama, USA.
Victor Darley-UsmarCenter for Free Radical Biology, Birmingham, Alabama, USA.
University of Alabama at Birmingham · US

Funding

Sex hormones and arthritis in a long lived animal modelP30AG050886 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DAVID B ALLISON · 2015 to 2026
$11.3M
Alpha-synuclein degradation mechanismsR01NS064090 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHANG, JIANHUA · 2010 to 2014
$1.6M
NIA NIH HHS P30 AG050886NINDS NIH HHS R01 NS064090
6 · The paper itself

Abstract

Parkinson's disease (PD) is a movement disorder with widespread neurodegeneration in the brain. Significant oxidative, reductive, metabolic, and proteotoxic alterations have been observed in PD postmortem brains. The alterations of mitochondrial function resulting in decreased bioenergetic health is important and needs to be further examined to help develop biomarkers for PD severity and prognosis. It is now becoming clear that multiple hits on metabolic and signaling pathways are likely to exacerbate PD pathogenesis. Indeed, data obtained from genetic and genome association studies have implicated interactive contributions of genes controlling protein quality control and metabolism. For example, loss of key proteins that are responsible for clearance of dysfunctional mitochondria through a process called mitophagy has been found to cause PD, and a significant proportion of genes associated with PD encode proteins involved in the autophagy-lysosomal pathway. In this review, we highlight the evidence for the targeting of mitochondria by proteotoxic, redox and metabolic stress, and the role autophagic surveillance in maintenance of mitochondrial quality. Furthermore, we summarize the role of α-synuclein, leucine-rich repeat kinase 2, and tau in modulating mitochondrial function and autophagy. Among the stressors that can overwhelm the mitochondrial quality control mechanisms, we will discuss 4-hydroxynonenal and nitric oxide. The impact of autophagy is context depend and as such can have both beneficial and detrimental effects. Furthermore, we highlight the potential of targeting mitochondria and autophagic function as an integrated therapeutic strategy and the emerging contribution of the microbiome to PD susceptibility.

Indexed as

AutophagyStress, PhysiologicalAnimalsHumansLysosomesMitochondriaMitophagyOxidative StressParkinson DiseaseSignal Transduction4-hydroxynonenalbioenergetic health indexendosome-lysosomesglucose metabolismmicrogliapost-translational modification

Identifiers

PMID29341130
PMCPMC5897151
OpenAlexW2791226661

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.