Evidence map›Paper›PMID 23024178›Full record

ReviewCold Spring Harbor perspectives in medicine2012

Drosophila as a model to study mitochondrial dysfunction in Parkinson's disease.

Ming Guo

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing 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

54 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Advances in understanding mitophagy's role in lung injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The mitophagy pathway and its implications in human diseases.Signal transduction and targeted therapy · 2023
    Review
  10. Article
  11. Genetic Reduction of Mitochondria Complex I Subunits is Protective against Cisplatin-Induced Neurotoxicity inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Review
  13. Article
  14. Autophagy in Drosophila and Zebrafish.Advances in experimental medicine and biology · 2021
    Article
  15. Article
  16. Article
  17. Mitophagy in cardiovascular homeostasis.Mechanisms of ageing and development · 2020
    Review
  18. Special Significance of Non-Frontiers in cell and developmental biology · 2020
    Review
  19. A Healthy Heart and a Healthy Brain: Looking at Mitophagy.Frontiers in cell and developmental biology · 2020
    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

1 author at 1 institution in 1 country.

Ming GuoDepartment of Neurology, Brain Research Institute, David Geffen School of Medicine, Los Angeles, California 90095, USA. mingfly@ucla.edu
University of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identification of single gene mutations that lead to inherited forms of Parkinson's disease (PD) has provided strong impetus for the use of animal models to study normal functions of these "PD genes" and the cellular defects that occur in the presence of pathogenic PD mutations. Drosophila has emerged as an effective model in PD-related gene studies. Important insights into the cellular basis of PD pathogenesis include the demonstration that two PD genes, PINK1 and parkin, function in a common pathway, with PINK1 positively regulating parkin, to control mitochondrial integrity and maintenance. This is accomplished through regulation of mitochondrial fission/fusion dynamics. Subsequent observations in both fly and mammalian systems showed that these proteins are important for sensing mitochondrial damage and recruiting damaged mitochondria to the quality-control machinery for subsequent removal. Here, I begin by reviewing the opportunities and challenges to understanding PD pathogenesis and developing new therapies. I then review the unique tools and technologies available in Drosophila for studying PD genes. Subsequently, I review lessons that we have learned from studies in Drosophila, emphasizing the PINK1/parkin pathway, as well as studies of DJ-1 and Omi/HtrA2, two additional genes associated with PD implicated in regulation of mitochondrial function. I end by discussing how Drosophila can be used to further probe the functions of PINK1 and parkin, and the regulation of mitochondrial quality more generally. In additional to PD, defects in mitochondrial function are associated with normal aging and with many diseases of aging. Thus, insights gained from the studies of mitochondrial dynamics and quality control in Drosophila are likely to be of general significance.

Indexed as

Disease Models, AnimalDrosophilaAnimalsDrosophila ProteinsGene Expression RegulationHigh-Temperature Requirement A Serine Peptidase 2HumansMitochondriaMitochondrial DynamicsMitophagyParkinson DiseaseProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseSerine EndopeptidasesUbiquitin-Protein LigasesDrosophila ProteinsHigh-Temperature Requirement A Serine Peptidase 2HtrA2 protein, Drosophilapark protein, DrosophilaPINK1 protein, DrosophilaProtein Serine-Threonine KinasesPTEN-Induced Putative KinaseSerine EndopeptidasesUbiquitin-Protein Ligases

Identifiers

PMID23024178
PMCPMC3543109
OpenAlexW2100004110

What OpenQuestion holds

Textmetadata
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.