Evidence map›Paper›PMID 31689437›Full record

ReviewJournal of molecular biology2020

Ubiquitin and Receptor-Dependent Mitophagy Pathways and Their Implication in Neurodegeneration.

Lauren E Fritsch, M Elyse Moore, Shireen A Sarraf, Alicia M Pickrell

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

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  11. Protective Effect of Lycopene on Ifosfamide-Induced Mitophagy throughInternational journal of fertility & sterility · 2025
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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

4 authors at 2 institutions in 1 country.

Lauren E FritschTranslational Biology, Medicine, and Health Graduate Program, Virginia Polytechnic Institute and State University, Roanoke, VA 24016, USA.
M Elyse MooreSchool of Neuroscience, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.
Shireen A SarrafBiochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Alicia M PickrellSchool of Neuroscience, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. Electronic address: alicia.pickrell@vt.edu.
Virginia Tech · USNational Institutes of Health · US

Funding

Intramural NIH HHS Z99 NS999999
6 · The paper itself

Abstract

Selective autophagy of mitochondria, or mitophagy, refers to the specific removal and degradation of damaged or surplus mitochondria via targeting to the lysosome for destruction. Disruptions in this homeostatic process may contribute to disease. The identification of diverse mitophagic pathways and how selectivity for each of these pathways is conferred is just beginning to be understood. The removal of both damaged and healthy mitochondria under disease and physiological conditions is controlled by either ubiquitin-dependent or receptor-dependent mechanisms. In this review, we will discuss the known types of mitophagy observed in mammals, recent findings related to PINK1/Parkin-mediated mitophagy (which is the most well-studied form of mitophagy), the implications of defective mitophagy to neurodegenerative processes, and unanswered questions inspiring future research that would enhance our understanding of mitochondrial quality control.

Indexed as

MitophagyAnimalsHumansMitochondriaNeurodegenerative DiseasesProtein KinasesPTEN-Induced Putative KinaseSignal TransductionUbiquitinUbiquitinated ProteinsUbiquitinationUbiquitin-Protein Ligasesparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitinUbiquitinated ProteinsUbiquitin-Protein LigasesAutophagosomeBNIP3L/NixMitochondriaPINK1/ParkinUbiquitin

Identifiers

PMID31689437
PMCPMC7195237
OpenAlexW2983495132

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.