ArticleMolecular neurobiology2024
SP1-Driven FOXM1 Upregulation Induces Dopaminergic Neuron Injury in Parkinson's Disease.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Colostrum extracellular vesicles are neuroprotective in models of Parkinson's disease.Theranostics · 2026Article
- Integrative bibliometric and transcriptomic analyses identify selenium-associated molecular signatures in the aging brain.Frontiers in aging neuroscience · 2026Article
- Function ofOncology letters · 2025Review
- Utility of the continuous spectrum formed by pathological states in characterizing disease properties.NPJ systems biology and applications · 2025Article
- Amyotrophic Lateral Sclerosis and Parkinson's Disease: Brain Tissue Transcriptome Analysis Reveals Interactions.Molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aberrant expression of Forkhead box M1 (FOXM1) has been associated with the pathological processes of Parkinson's disease (PD), but the upstream and downstream regulators remain poorly understood. This study sought to examine the underlying mechanism of FOXM1 in dopaminergic neuron injury in PD. Bioinformatics analysis was conducted to pinpoint the differential expression of FOXM1, which was verified in the nigral tissues of rotenone-lesioned mice and dopaminergic neuron MN9D cells. Interactions among SP1, FOXM1, SNAI2, and CXCL12 were analyzed. To evaluate their effects on dopaminergic neuron injury, the lentiviral vector-mediated manipulation of FOXM1, SP1, and CXCL12 was introduced in rotenone-lesioned mice and MN9D cells. SP1, FOXM1, SNAI2, and CXCL12 abundant expression occurred in rotenone-lesioned mice and MN9D cells. Silencing of FOXM1 delayed the rotenone-induced dopaminergic neuron injury in vitro. Mechanistically, SP1 was an upstream transcription factor of FOXM1 and upregulated FOXM1 expression, leading to increased SNAI2 and CXCL12 expression. In vivo, data confirmed that SP1 promoted dopaminergic neuron injury by activating the FOXM1/SNAI2/CXCL12 axis. Our data indicate that SP1 silencing has neuroprotective effects on dopaminergic neurons, which is dependent upon the inactivated FOXM1/SNAI2/CXCL12 axis.
Indexed as
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38200349What Socratic 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 Socratic graph.