Evidence map›Paper›PMID 33067655›Full record

ReviewCellular and molecular life sciences : CMLS2021

Selective autophagy as a therapeutic target for neurological diseases.

Weilin Xu, Umut Ocak, Liansheng Gao, Sheng Tu, Cameron J Lenahan, Jianmin Zhang, Anwen Shao

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.8field-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

46 citing papers in PubMed, 81 citations in OpenAlex.

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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

7 authors at 4 institutions in 2 countries.

Weilin Xu *Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Umut Ocak *Department of Emergency Medicine, Bursa Yuksek Ihtisas Training and Research Hospital, University of Health Sciences, 16310, Bursa, Turkey.
Liansheng Gao *Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Sheng TuState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310009, Zhejiang, China.
Cameron J LenahanBurrell College of Osteopathic Medicine, Las Cruces, NM, USA.
Jianmin ZhangDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. zjm135@zju.edu.cn.
Anwen ShaoDepartment of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. 21118116@zju.edu.cn.ORCID http://orcid.org/0000-0001-9986-6290
Second Affiliated Hospital of Zhejiang University · CNBursa Technical University · TRChinese Institute for Brain Research · CNZhejiang University · CN

Funding

National Basic Research Program of China (973 Program) 2017YFC1308500National Natural Science Foundation of China 81371433National Natural Science Foundation of China 81701144Zhejiang Provincial Key Laboratory of Wood Science and Technology (CN) 2017C03021
6 · The paper itself

Abstract

The neurological diseases primarily include acute injuries, chronic neurodegeneration, and others (e.g., infectious diseases of the central nervous system). Autophagy is a housekeeping process responsible for the bulk degradation of misfolded protein aggregates and damaged organelles through the lysosomal machinery. Recent studies have suggested that autophagy, particularly selective autophagy, such as mitophagy, pexophagy, ER-phagy, ribophagy, lipophagy, etc., is closely implicated in neurological diseases. These forms of selective autophagy are controlled by a group of important proteins, including PTEN-induced kinase 1 (PINK1), Parkin, p62, optineurin (OPTN), neighbor of BRCA1 gene 1 (NBR1), and nuclear fragile X mental retardation-interacting protein 1 (NUFIP1). This review highlights the characteristics and underlying mechanisms of different types of selective autophagy, and their implications in various forms of neurological diseases.

Indexed as

Molecular Targeted TherapyAutophagyCell Cycle ProteinsHumansIntracellular Signaling Peptides and ProteinsMembrane Transport ProteinsNervous System DiseasesNuclear ProteinsProtein KinasesPTEN-Induced Putative KinaseRNA-Binding ProteinsUbiquitin-Protein LigasesCell Cycle ProteinsIntracellular Signaling Peptides and ProteinsMembrane Transport ProteinsNBR1 protein, humanNuclear ProteinsNUFIP1 protein, humanOPTN protein, humanP62 protein, humanparkin proteinProtein KinasesPTEN-Induced Putative KinaseRNA-Binding ProteinsUbiquitin-Protein LigasesAlzheimer’s diseaseAutophagy receptorMacroautophagyNeuroprotectionParkinson’s diseaseStroke

Identifiers

PMID33067655
PMCPMC7904548
OpenAlexW3092994647

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.