ArticleOxidative medicine and cellular longevity2022
Bioinformatic Analysis of Genetic Factors from Human Blood Samples and Postmortem Brains in Parkinson's Disease.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 48 citations in OpenAlex.
- Disrupted TFEB/GDNF-cAMP/ATP Coupling Underlies Astrocytic Dysfunction and Depression in LRRK2 G2019S Parkinson's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Naringenin protects against renal ischemia-reperfusion injury following unilateral nephrectomy via modulation of oxidative stress and kisspeptin expression.International urology and nephrology · 2026Article
- Targeting NLRP3 inflammasome to mitigate chemotherapy-induced cardiotoxicity: advances in selective inhibitors and natural modulators.Molecular biology reports · 2026Review
- Single-cell analysis of the peripheral immune landscape in Parkinson's disease: insights into dendritic cell and CD4+ T-cell transcriptomics.NPJ Parkinson's disease · 2026Article
- Astrocyte Autophagy in Neurodegenerative Diseases: Current Progress in Mechanisms and Therapeutics.Neurochemical research · 2025Review
- Large-scale plasma proteomics uncovers preclinical molecular signatures of Parkinson's disease and overlap with other neurodegenerative disorders.medRxiv : the preprint server for health sciences · 2025Article
- Immune Cell Proteins and Parkinson's Disease: A Mendelian Randomization Analysis of Causal Associations.Brain and behavior · 2025Article
- Is periodontitis triggering an inflammatory response in the liver, and does this reaction entail oxidative stress?Odontology · 2025Review
- Uncovering naringin's anticancer mechanisms in glioblastoma via molecular docking and network pharmacology approaches.Scientific reports · 2024Article
- DL-3-n-Butylphthalide Ameliorates Post-stroke Emotional Disorders by Suppressing Neuroinflammation and PANoptosis.Neurochemical research · 2024Article
- Byrsonima sericea Ethanol Extract Protected PC12 Cells from the Oxidative Stress and Apoptosis Induced by 6-Hydroxydopamine.Neurochemical research · 2024Article
- Grid2 interacting protein is a potential biomarker related to immune infiltration in colorectal cancer.European journal of medical research · 2023Article
- LRRK2 Gly2019Ser Mutation Promotes ER Stress via Interacting with THBS1/TGF-β1 in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Association between oxidative balance score and urinary incontinence in females: results from the national health and nutrition examination survey in 2005-2018.International urology and nephrology · 2023Article
- Itaconate: A Potent Macrophage Immunomodulator.Inflammation · 2023Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the most prevalent neurodegenerative disorders characterized by motor and nonmotor symptoms due to the selective loss of midbrain dopaminergic neurons. Pharmacological and surgical interventions have not been possible to cure PD; however, the cause of neurodegeneration remains unclear. Here, we performed and tested a multitiered bioinformatic analysis using the GEO and Proteinexchange database to investigate the gene expression involved in the pathogenesis of PD. Then we further validated individual differences in gene expression in whole blood samples that we collected in the clinic. We also made an interaction analysis and prediction for these genetic factors. There were in all 1045 genes expressing differently in PD compared with the healthy control group. Protein-protein interaction (PPI) networks showed 10 top hub genes: ACO2, MDH2, SDHA, ATP5A1, UQCRC2, PDHB, SUCLG1, NDUFS3, UQCRC1, and ATP5C1. We validated the ten hub gene expression in clinical PD patients and showed the expression of MDH2 was significantly different compared with healthy control. Besides, we also identified the expression of G6PD, GRID2, RIPK2, CUL4B, BCL6, MRPS31, GPI, and MAP 2 K1 were all significantly increased, and levels of MAPK, ELAVL1, RAB14, KLF9, ARF1, ARFGAP1, ATG7, ABCA7, SFT2D2, E2F2, MAPK7, and UHRF1 were all significantly decreased in PD. Among them, to our knowledge, we presently have the most recent and conclusive evidence that GRID2, RIPK2, CUL4B, E2F2, and ABCA7 are possible PD indicators. We confirmed several genetic factors which may be involved in the pathogenesis of PD. They could be promising markers for discriminating the PD and potential factors that may affect PD development.
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