Evidence map›Paper›PMID 34362731›Full record

ArticleScience advances2021

Longitudinal tracking of neuronal mitochondria delineates PINK1/Parkin-dependent mechanisms of mitochondrial recycling and degradation.

Huihui Li, Zak Doric, Amandine Berthet, Danielle M Jorgens, Mai K Nguyen, Ivy Hsieh, Julia Margulis, Rebecca Fang, Jayanta Debnath, Hiromi Sesaki and 3 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.4field-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

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Neural cell state modulation bybioRxiv : the preprint server for biology · 2026
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  3. Molecular biology of the cell · 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

13 authors at 4 institutions in 1 country.

Huihui LiGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0002-4469-3705
Zak DoricGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0003-2608-4196
Amandine BerthetGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0002-8529-6562
Danielle M JorgensElectron Microscope Laboratory, University of California, Berkeley, Berkeley, CA 94720, USA.ORCID http://orcid.org/0000-0002-7143-0118
Mai K NguyenGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0003-3550-7728
Ivy HsiehDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Julia MargulisGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.
Rebecca FangGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0001-7920-2796
Jayanta DebnathDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.ORCID http://orcid.org/0000-0002-8745-4069
Hiromi SesakiDepartment of Cell Biology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Steve FinkbeinerGraduate Program in Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0002-3480-394X
Eric HuangGraduate Program in Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA.ORCID http://orcid.org/0000-0002-5381-3801
Ken NakamuraGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA. ken.nakamura@gladstone.ucsf.edu.ORCID http://orcid.org/0000-0002-9192-182X
Gladstone Institutes · USUniversity of California, San Francisco · USJohns Hopkins University · USUniversity of California, Berkeley · US

Funding

Dysfunction of the Autophagy-Lysosomal Pathway as a Common Mechanism of NeurodegenerationRF1AG058476 · NIA · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2017 to 2018
$4.1M
Tauopathy in AD and FTD - Molecular Determinants of Phenotypic DiversityRF1AG056151 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CARLSON, GEORGE A., DUFF, KAREN · 2017 to 2017
$4.1M
Determining how neural activity impairs bioenergetics in PD pathogenesisR01NS091902 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI NAKAMURA, KEN · 2015 to 2019
$2.1M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
Mechanisms of HIPK2 in neurodegenerationR01NS098516 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2016 to 2020
$1.7M
Novel Therapeutic Approaches to Alzheimer's DiseaseP30NS069496 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2009 to 2010
$1.7M
Recruiting & Retaining Older African Americans into Research (ROAR)R24AG065151 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MITCHELL, JAYMIA ANN · 2020 to 2022
$1.3M
Mechanisms of ER Stress and Neurodegeneration in Parkinson's DiseaseI01BX001108 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI Eric J Huang · 2011 to 2026
–
BLRD VA I01 BX001108NCRR NIH HHS C06 RR018928NIA NIH HHS R24 AG065151NIA NIH HHS RF1 AG056151NIA NIH HHS RF1 AG058476NINDS NIH HHS P30 NS069496NINDS NIH HHS R01 NS091902NINDS NIH HHS R01 NS098516Wellcome Trust
6 · The paper itself

Abstract

Altered mitochondrial quality control and dynamics may contribute to neurodegenerative diseases, including Parkinson's disease, but we understand little about these processes in neurons. We combined time-lapse microscopy and correlative light and electron microscopy to track individual mitochondria in neurons lacking the fission-promoting protein dynamin-related protein 1 (Drp1) and delineate the kinetics of PINK1-dependent pathways of mitochondrial quality control. Depolarized mitochondria recruit Parkin to the outer mitochondrial membrane, triggering autophagosome formation, rapid lysosomal fusion, and Parkin redistribution. Unexpectedly, these mitolysosomes are dynamic and persist for hours. Some are engulfed by healthy mitochondria, and others are deacidified before bursting. In other cases, Parkin is directly recruited to the matrix of polarized mitochondria. Loss of PINK1 blocks Parkin recruitment, causes LC3 accumulation within mitochondria, and exacerbates Drp1KO toxicity to dopamine neurons. These results define a distinct neuronal mitochondrial life cycle, revealing potential mechanisms of mitochondrial recycling and signaling relevant to neurodegeneration.

Identifiers

PMID34362731
PMCPMC8346224
OpenAlexW3192276836

What OpenQuestion holds

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Registered trials

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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.