Evidence map›Paper›PMID 34729301›Full record

ReviewActa pharmaceutica Sinica. B2021

Targeting autophagy using small-molecule compounds to improve potential therapy of Parkinson's disease.

Kai Zhang, Shiou Zhu, Jiamei Li, Tingting Jiang, Lu Feng, Junping Pei, Guan Wang, Liang Ouyang, Bo Liu

Open access · diamondAbstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
12.2field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

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  11. Nervonic Acid fromBiomaterials research · 2026
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9 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Kai ZhangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Shiou ZhuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Jiamei LiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Tingting JiangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Lu FengState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Junping PeiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Guan WangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Liang OuyangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Bo LiuState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD), known as one of the most universal neurodegenerative diseases, is a serious threat to the health of the elderly. The current treatment has been demonstrated to relieve symptoms, and the discovery of new small-molecule compounds has been regarded as a promising strategy. Of note, the homeostasis of the autolysosome pathway (ALP) is closely associated with PD, and impaired autophagy may cause the death of neurons and thereby accelerating the progress of PD. Thus, pharmacological targeting autophagy with small-molecule compounds has been drawn a rising attention so far. In this review, we focus on summarizing several autophagy-associated targets, such as AMPK, mTORC1, ULK1, IMPase, LRRK2, beclin-1, TFEB, GCase, ERR

Indexed as

3-MA, 3-methyladenine5-HT2A, Serotonin 2A5-HT2C, serotonin 2CA2A, adenosine 2AAADC, aromatic amino acid decarboxylaseALP, autophagy-lysosomal pathwayAMPK, 5ʹAMP-activated protein kinaseATG, autophagy related proteinATP13A2, ATPase cation transporting 13A2ATTEC, autophagosome-tethering compoundAUC, the area under the curveAUTAC, autophagy targeting chimeraAutophagyBAF, bafilomycinA1BBB, blood−brain barrierCL, clearance rateCMA, chaperone-mediated autophagyCNS, central nervous systemCOMT, catechol-O-methyltransferaseDA, dopamineDAT, dopamine transporterDJ-1, Parkinson protein 7DR, dopamine receptorER, endoplasmic reticulumERRα, estrogen-related receptor alphaF, oral bioavailabilityGAPDH, glyceraldehyde 3-phosphate dehydrogenaseGBA, glucocerebrosidase β acidGWAS, genome-wide association studyHDAC6, histone deacetylase 6HSC70, heat shock cognate 71 kDa proteinHSPA8, heat shock 70 kDa protein 8IMPase, inositol monophosphataseIPPase, inositol polyphosphate 1-phosphataseKI, knockinLAMP2A, lysosome-associated membrane protein 2 ALamp2a, type 2A lysosomal-associated membrane proteinLC3, light chain 3LIMP-2, lysosomal integrated membrane protein-2LRRK2, leucine-rich repeat sequence kinase 2LRS, leucyl-tRNA synthetaseLUHMES, lund human mesencephalicmAChR, muscarinic acetylcholine receptorMAO-B, monoamine oxidase BMPP+, 1-methyl-4-phenylpyridiniumMPTP, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridinemTOR, the mammalian target of rapamycinMYCBP2, MYC-binding protein 2NMDA, N-methyl-d-aspartic acidONRs, orphan nuclear receptorsParkin, parkin RBR E3 ubiquitin−protein ligaseParkinson's disease (PD)PDE4, phosphodiesterase 4PD, Parkinson's diseasePD therapyPI3K, phosphatidylinositol 3-kinasePI3P, phosphatidylinositol 3-phosphatePINK1, PTEN-induced kinase 1PLC, phospholipase CPREP, prolyl oligopeptidaseROS, reactive oxygen speciesSAR, structure–activity relationshipSAS, solvent accessible surfaceSmall-molecule compoundSNCA, α-synuclein geneSN, substantia nigraSYT11, synaptotagmin 11TargetTFEB, transcription factor EBTSC2, tuberous sclerosis complex 2ULK1, UNC-51-like kinase 1UPS, ubiquitin−proteasome systemα-syn, α-synuclein

Identifiers

PMID34729301
PMCPMC8546670
OpenAlexW3135016317

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.