Evidence map›Paper›PMID 24178442›Full record

ArticleAutophagy2014

HMGB1 is involved in autophagy inhibition caused by SNCA/α-synuclein overexpression: a process modulated by the natural autophagy inducer corynoxine B.

Ju-Xian Song, Jia-Hong Lu, Liang-Feng Liu, Lei-Lei Chen, Siva Sundara Kumar Durairajan, Zhenyu Yue, Hong-Qi Zhang, Min Li

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 3 pooled it
6.1field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 3 syntheses or guidelines pooled it, 153 citations in OpenAlex.

  1. Pooled it
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  8. Current issues in molecular biology · 2025
    Article
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  17. The beneficial pharmacological effects ofFrontiers in pharmacology · 2024
    Review
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Ju-Xian SongSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong.
Jia-Hong LuSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong; Departments of Neurology and Neuroscience; Friedman Brain Institute; Icahn School of Medicine at Mount Sinai; New York, NY USA.
Liang-Feng LiuSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong.
Lei-Lei ChenSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong.
Siva Sundara Kumar DurairajanSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong.
Zhenyu YueDepartments of Neurology and Neuroscience; Friedman Brain Institute; Icahn School of Medicine at Mount Sinai; New York, NY USA.
Hong-Qi ZhangSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong.
Min LiSchool of Chinese Medicine; Hong Kong Baptist University; Kowloon Tong; Hong Kong.
Kowloon Hospital · CNIcahn School of Medicine at Mount Sinai · USHong Kong Baptist University · HK

Funding

Neuronal Autophagy: a Cell-Autonomous Protection MechanismR01NS060123 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Zhenyu Yue · 2008 to 2026
$9.2M
NINDS NIH HHS R01 NS060123
6 · The paper itself

Abstract

SNCA/α-synuclein and its rare mutations are considered as the culprit proteins in Parkinson disease (PD). Wild-type (WT) SNCA has been shown to impair macroautophagy in mammalian cells and in transgenic mice. In this study, we monitored the dynamic changes in autophagy process and confirmed that overexpression of both WT and SNCA(A53T) inhibits autophagy in PC12 cells in a time-dependent manner. Furthermore, we showed that SNCA binds to both cytosolic and nuclear high mobility group box 1 (HMGB1), impairs the cytosolic translocation of HMGB1, blocks HMGB1-BECN1 binding, and strengthens BECN1-BCL2 binding. Deregulation of these molecular events by SNCA overexpression leads to autophagy inhibition. Overexpression of BECN1 restores autophagy and promotes the clearance of SNCA. siRNA knockdown of Hmgb1 inhibits basal autophagy and abolishes the inhibitory effect of SNCA on autophagy while overexpression of HMGB1 restores autophagy. Corynoxine B, a natural autophagy inducer, restores the deficient cytosolic translocation of HMGB1 and autophagy in cells overexpressing SNCA, which may be attributed to its ability to block SNCA-HMGB1 interaction. Based on these findings, we propose that SNCA-induced impairment of autophagy occurs, in part, through HMGB1, which may provide a potential therapeutic target for PD.

Indexed as

Alkaloidsalpha-SynucleinAnimalsApoptosis Regulatory ProteinsAutophagyBeclin-1Cell SurvivalCytosolGene Knockdown TechniquesHMGB1 ProteinHumansIndole AlkaloidsLysosomesMiceModels, BiologicalMutant ProteinsAlkaloidsalpha-SynucleinApoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratcorynoxeineHMGB1 ProteinIndole AlkaloidsMutant ProteinsProteasome Endopeptidase Complexautophagycorynoxine BHMGB1Parkinson diseaseSNCA

Identifiers

PMID24178442
PMCPMC4389868
OpenAlexW2009839229

What OpenQuestion holds

Textmetadata
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.