Evidence map›Paper›PMID 27911343›Full record

ReviewJournal of Parkinson's disease2017

PINK1, Parkin, and Mitochondrial Quality Control: What can we Learn about Parkinson's Disease Pathobiology?

Dominika Truban, Xu Hou, Thomas R Caulfield, Fabienne C Fiesel, Wolfdieter Springer

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of Parkinson's disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 2 pooled it
14.3field-weighted citation impact, top 1% 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

146 citing papers in PubMed, 2 syntheses or guidelines pooled it, 231 citations in OpenAlex.

  1. Rethinking 'rare'Journal of Parkinson's disease · 2025
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A.Molecular neurodegeneration advances · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Genome-wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  19. Article
  20. Article

86 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Dominika TrubanDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Xu HouDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Thomas R CaulfieldDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Fabienne C FieselDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Wolfdieter SpringerDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Jacksonville College · USMayo Clinic in Florida · US

Funding

Molecular mechanisms of Parkin-directed mitochondrial quality controlR01NS085070 · NINDS · MAYO CLINIC JACKSONVILLE · PI SPRINGER, WOLFDIETER · 2014 to 2018
$1.7M
NINDS NIH HHS R01 NS085070
6 · The paper itself

Abstract

The first clinical description of Parkinson's disease (PD) will embrace its two century anniversary in 2017. For the past 30 years, mitochondrial dysfunction has been hypothesized to play a central role in the pathobiology of this devastating neurodegenerative disease. The identifications of mutations in genes encoding PINK1 (PTEN-induced kinase 1) and Parkin (E3 ubiquitin ligase) in familial PD and their functional association with mitochondrial quality control provided further support to this hypothesis. Recent research focused mainly on their key involvement in the clearance of damaged mitochondria, a process known as mitophagy. It has become evident that there are many other aspects of this complex regulated, multifaceted pathway that provides neuroprotection. As such, numerous additional factors that impact PINK1/Parkin have already been identified including genes involved in other forms of PD. A great pathogenic overlap amongst different forms of familial, environmental and even sporadic disease is emerging that potentially converges at the level of mitochondrial quality control. Tremendous efforts now seek to further detail the roles and exploit PINK1 and Parkin, their upstream regulators and downstream signaling pathways for future translation. This review summarizes the latest findings on PINK1/Parkin-directed mitochondrial quality control, its integration and cross-talk with other disease factors and pathways as well as the implications for idiopathic PD. In addition, we highlight novel avenues for the development of biomarkers and disease-modifying therapies that are based on a detailed understanding of the PINK1/Parkin pathway.

Indexed as

AnimalsHumansMitochondriaParkinson DiseaseProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligasesparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesmitochondriamitophagyParkinParkinson’s diseasePINK1ubiquitin

Identifiers

PMID27911343
PMCPMC5302033
OpenAlexW2557944616

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.