ReviewMolecular neurobiology2025
The Potential Roles of HSPA2 in Parkinson's Disease.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder traditionally identified by its characteristic motor symptoms, the presence of Lewy bodies, and the loss of neurons in the substantia nigra. At present, there is no cure for the disease. Our study aimed to uncover the new aspects of the pathogenesis underlying PD. Firstly, we identified that HSPA2 is potentially involved in the PD pathogenesis through a bioinformatic approach; HSPA2 was associated with the disease duration. For that, we analyzed the correlation of the clinical information of patients with the HSPA2 gene expression level. Then, the expression of HSPA2 was investigated in vivo using the midbrain from the MPTP-treated mouse models. The HSPA2 levels significantly increased in the midbrain tissue from the PD mouse models. The mechanistic studies about HSPA2 in the pathogenesis of PD were conducted in vitro in the HEK293T cell line, which observed the changes in α-synuclein expression by regulating the HSPA2 expression. In the HEK293T cell line, the overexpression of HSPA2 increased the α-synuclein aggregates formation, and the knockdown of HSPA2 reduced the α-synuclein aggregates accumulation. Therefore, this study hypothesized that HSPA2 might be a new regulator of α-synuclein associated with the PD pathology.
Indexed as
Identifiers
41264038What OpenQuestion holds
Registered trials
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.