Evidence map›Paper›PMID 40287631›Full record

ReviewMolecular medicine (Cambridge, Mass.)2025

The interplay of iron, oxidative stress, and α-synuclein in Parkinson's disease progression.

Yan Chen, Xixi Luo, Yukun Yin, Elizabeth Rosalind Thomas, Kezhi Liu, Wenjun Wang, Xiang Li

Abstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  5. Synthetic Cyclic CAntioxidants (Basel, Switzerland) · 2026
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  8. Article
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  15. Article
  16. Impact of Oxidative Stress-Driven Ferroptosis in Neurodegeneration.International journal of molecular sciences · 2026
    Review
  17. Article
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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

7 authors.

Yan Chen *Department of Psychiatry, The Affiliated Zigong Hospital, Zigong Mental Health Center, Zigong Institute of Brain Science, Southwest Medical University, Luzhou, 646000, China.
Xixi Luo *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China.
Yukun Yin *Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China.
Elizabeth Rosalind ThomasDepartment of Medical Microbiology, PGIMER, Chandigarh, 160012, India.
Kezhi LiuDepartment of Psychiatry, The Affiliated Zigong Hospital, Zigong Mental Health Center, Zigong Institute of Brain Science, Southwest Medical University, Luzhou, 646000, China.
Wenjun WangDepartment of Psychiatry, The Affiliated Zigong Hospital, Zigong Mental Health Center, Zigong Institute of Brain Science, Southwest Medical University, Luzhou, 646000, China. wenjunwang1213@126.com.
Xiang LiDepartment of Psychiatry, The Affiliated Zigong Hospital, Zigong Mental Health Center, Zigong Institute of Brain Science, Southwest Medical University, Luzhou, 646000, China. lix2009@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The irreversible degeneration of dopamine neurons induced by α-synuclein (α-syn) aggregation in the substantia nigra is the central pathological feature of Parkinson's disease (PD). Neuroimaging and pathological autopsy studies consistently confirm significant iron accumulation in the brain of PD patients, suggesting a critical role for iron in disease progression. Current research has established that iron overload induces ferroptosis in dopaminergic neurons, evidence indicates that the impact of iron on PD pathology extends beyond ferroptosis. Iron also plays a regulatory role in modulating α-syn, affecting its aggregation, spatial conformation, post-translational modifications, and mRNA stability. Iron-induced α-syn aggregation can contribute to dopaminergic neurodegeneration through additional mechanisms, potentially creating a feedback loop in which α-syn further enhances iron accumulation, thus perpetuating a vicious cycle of neurotoxicity. Given α-syn's intrinsically disordered structure, targeting iron metabolism presents a promising therapeutic strategy for PD. Therefore, the development of iron chelators, alone or in combination with other therapeutic drugs, may offer a beneficial approach to alleviating PD symptoms and slowing disease progression.

Indexed as

alpha-SynucleinIronOxidative StressParkinson DiseaseAnimalsDisease ProgressionDopaminergic NeuronsFerroptosisHumansalpha-SynucleinIronFerroptosisIronParkinson's diseaseα-synuclein

Identifiers

PMID40287631
PMCPMC12034127

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.