Evidence map›Paper›PMID 32296327›Full record

ArticleFrontiers in aging neuroscience2020

Pharmacological Inhibition of HDAC6 Attenuates NLRP3 Inflammatory Response and Protects Dopaminergic Neurons in Experimental Models of Parkinson's Disease.

Shaoqi Yan, Xinbing Wei, Wencheng Jian, Yue Qin, Jia Liu, Shaowei Zhu, Fan Jiang, Haiyan Lou, Bin Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2020. 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
4.0field-weighted citation impact, top 6% 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, 75 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

9 authors at 2 institutions in 1 country.

Shaoqi YanDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Xinbing WeiDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Wencheng JianDepartment of Radiology, Qilu Hospital, Shandong University, Jinan, China.
Yue QinDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Jia LiuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Shaowei ZhuDepartment of Neurology, Qilu Hospital, Shandong University, Jinan, China.
Fan JiangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Haiyan LouDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Bin ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the role of histone deacetylase 6 (HDAC6) deacetylation activity in nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammatory response and explore the effects of pharmacological inhibition of HDAC6 with tubastatin A (TBA) on dopaminergic injury.

methodsUsing 6-OHDA-induced Parkinson's disease (PD) models, we examined the effects of TBA on NLRP3 activation and cell injury in SH-SY5Y cells. We also investigated the effects of TBA on NLRP3 inflammatory responses and dopaminergic injury in the nigrostriatal system in mice and analyzed the acetylation levels of peroxiredoxin2 (Prx2) and oxidative stress.

resultsTBA inhibited 6-OHDA-induced NLRP3 activation, as demonstrated by decreased expressions of NLRP3 and matured caspase-1 and IL-1β, and also alleviated glial proliferation and dopaminergic neuronal degeneration. Notably, TBA recovered acetylation levels of Prx2 and reduced oxidative stress.

conclusionOur findings indicate that pharmacological inhibition of HDAC6 with TBA attenuates NLRP3 inflammation and protects dopaminergic neurons, probably through Prx2 acetylation. This study suggests that the deacetylase catalytic domain of HDAC6 is a potential target for PD treatment.

Indexed as

HDAC6NLRP3Parkinson’s diseaseperoxiredoxin 2tubastatin A

Identifiers

PMID32296327
PMCPMC7137996
OpenAlexW3015051404

What OpenQuestion holds

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LicenceCC BY
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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.