Evidence map›Paper›PMID 29626647›Full record

ReviewNeuroscience letters2019

Multiple pathways for mitophagy: A neurodegenerative conundrum for Parkinson's disease.

Charleen T Chu

Abstract readReview
In one paragraph

Review in Neuroscience letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Molecular mechanisms underlying FCCP-induced mitophagy in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026
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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.

Charleen T ChuDepartments of Pathology and Ophthalmology, Pittsburgh Institute for Neurodegenerative Diseases, McGowan Institute for Regenerative Medicine and Center for Neuroscience at the University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: ctc4@pitt.edu.
University of Pittsburgh · US

Funding

Regulation of Autophagy & Mitochondrial Recycling in Neuronal Cell Death- SupplementR01AG026389 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2007 to 2024
$6.0M
Dendrite regulation by the mitochondrial kinase PINK1: Implications for PD/LBD Diversity SupplementR01NS101628 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Charleen T Chu, Zachary P Wills · 2017 to 2026
$4.0M
PINK1 Regulation of Neuronal and Mitochondrial HomeostasisR01NS065789 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2011 to 2014
$1.3M
PINK1 Regulation of Neuronal and Mitochondrial HomeostasisR56NS065789 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHU, CHARLEEN T · 2010 to 2016
$813k
NIA NIH HHS R01 AG026389NINDS NIH HHS R01 NS065789NINDS NIH HHS R01 NS101628NINDS NIH HHS R56 NS065789
6 · The paper itself

Abstract

It has been nearly a decade since the first landmark studies implicating familial recessive Parkinson's disease genes in the regulation of selective mitochondrial autophagy. The PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase Parkin (encoded by the PARK2 gene) act together to mark depolarized mitochondria for degradation. There is now an extensive body of literature detailing key mediators and steps in this pathway, based mostly on work in transformed cell lines. However, the degree to which PINK1-triggered mitophagy contributes to mitochondrial quality control in the mammalian brain, and the extent to which its disruption contributes to Parkinson's disease pathogenesis remain uncertain. In recent years, it has become clear that there are multiple, potentially redundant, pathways of cargo specification for mitophagy. Important mitophagy-independent functions of PINK1 and Parkin are also emerging. This review summarizes key features of three major mitophagy cargo recognition systems: receptor-mediated, ubiquitin-mediated and cardiolipin-mediated. New animal models that may be useful for tracking the delivery of mitochondria into lysosomes in different neuronal populations will be highlighted. Combining these research tools with methods to selectively disrupt specific mitophagy pathways may lead to a better understanding of the potential role of mitophagy in modulating neuronal vulnerability in Parkinson's spectrum (PD/PDD/DLB) and other neurodegenerative diseases.

Indexed as

AnimalsAutophagyHumansMitochondriaMitophagyNeuronsParkinson DiseaseAutophagyDementia with Lewy bodiesMitochondriaMitophagyNeurodegenerationParkinson’s diseaseParkinson’s disease dementia

Identifiers

PMID29626647
PMCPMC6170746
OpenAlexW2795996015

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.