Evidence map›Paper›PMID 39553632›Full record

ArticleHeliyon2024

SHANK2-AS3: A potential biomarker for Parkinson's disease and its role in neuronal apoptosis via NF-κB signaling in SH-SY5Y cells.

Qiong Huang, Dani Qin, Chunyan Chen, Yu Kang, Haocong Chen, Min Xu, Rao Fu, Xiaohua Dong

Abstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

8 authors.

Qiong HuangHongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Dani QinDepartment of Pediatrics, Yixing People's Hospital, No.75 Tongzhenguan Road, Yixing, Jiangsu, 214200, China.
Chunyan ChenDepartment of Neurology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu KangHongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Haocong ChenHongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Min XuDepartment of Neurology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Rao FuDepartment of Neurology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaohua DongHongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder primarily driven by the degeneration of dopaminergic neurons, manifesting as hallmark symptoms such as muscle rigidity, tremors, and motor dysfunction, all of which severely compromise patients' quality of life. Increasing evidence highlights the critical role of long non-coding RNAs (lncRNAs) in PD pathogenesis. However, the specific involvement of SHANK2-AS3 in PD remains unclear. By reanalyzing the dysregulated lncRNAs from the GSE22491 dataset, we identified a significant upregulation of SHANK2-AS3 in PD patients compared to healthy controls. This finding was further validated in a new cohort of PD patients, where SHANK2-AS3 expression was notably elevated in peripheral blood samples. Additionally, we observed a marked increase in SHANK2-AS3 expression in MPTP-treated SH-SY5Y cells, a commonly used

Indexed as

Cell apoptosisParkinson's diseaseSHANK2-AS3

Identifiers

PMID39553632
PMCPMC11564949

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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.