Evidence map›Paper›PMID 23533695›Full record

ReviewOxidative medicine and cellular longevity2013

Function and characteristics of PINK1 in mitochondria.

Satoru Matsuda, Yasuko Kitagishi, Mayumi Kobayashi

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026
    Review
  6. Article
  7. Article
  8. [PINK1 suppresses colorectal cancer cell growth through epigenetic regulation of histone modifications].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Article
  9. Review
  10. Protective Effect of Lycopene on Ifosfamide-Induced Mitophagy throughInternational journal of fertility & sterility · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Mass spectrometry-based proteomics for biomarker discovery in theNeuroprotection (Chichester, England) · 2024
    Review
  17. Review
  18. Review
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Satoru MatsudaDepartment of Environmental Health Science, Nara Women's University, Kita-Uoya Nishimachi, Nara 630-8506, Japan. smatsuda@cc.nara-wu.ac.jp
Yasuko Kitagishi
Mayumi Kobayashi
Nara Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in phosphatase and tensin homologue-induced kinase 1 (PINK1) cause recessively inherited Parkinson's disease, a neurodegenerative disorder linked to mitochondrial dysfunction. Studies support the notion of neuroprotective roles for the PINK1, as it protects cells from damage-mediated mitochondrial dysfunction, oxidative stress, and cell apoptosis. PARL is a mitochondrial resident rhomboid serine protease, and it has been reported to mediate the cleavage of the PINK1. Interestingly, impaired mitophagy, an important autophagic quality control mechanism that clears the cells of damaged mitochondria, may also be an underlying mechanism of disease pathogenesis in patients for Parkinson's disease with the PARL mutations. Functional studies have revealed that PINK1 recruits Parkin to mitochondria to initiate the mitophagy. PINK1 is posttranslationally processed, whose level is definitely regulated in healthy steady state of mitochondria. As a consequence, PINK1 plays a pivotal role in mitochondrial healthy homeostasis.

Indexed as

ApoptosisHumansMitochondriaMutationNeurodegenerative DiseasesProtein KinasesPTEN-Induced Putative KinaseProtein KinasesPTEN-Induced Putative Kinase

Identifiers

PMID23533695
PMCPMC3600171
OpenAlexW2019146253

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.