ReviewInternational journal of molecular sciences2025
Parkinson's Disease: The Neurodegenerative Enigma Under the "Undercurrent" of Endoplasmic Reticulum Stress.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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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
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Actual Data on Essential Trace Elements in Parkinson's Disease.Nutrients · 2025Pooled it
- Lycium Barbarum Polysaccharides Alleviate Parkinson's Disease-Induced Neurodegeneration by Up-Regulating USP10 to Modulate Endoplasmic Reticulum Stress.Neurochemical research · 2026Article
- Biogenesis of TNF-α-insights into proteostasis and inflammation.The FEBS journal · 2026Review
- Ginsenoside Rg1, a Natural Lysosomal Enhancer, Alleviates Parkinson's Disease Pathology via Cathepsin D-Dependent Regulation of α-Synuclein Homeostasis.Phytotherapy research : PTR · 2026Article
- Mitochondrial ROS in Retinal Neurodegeneration: Thresholds, Quality Control Failure, and Precision Therapeutic Windows.Biomolecules · 2026Review
- Exosome-derived CDNF Inhibits Astrocyte and T Cell Activation by Regulating HSPA5 and Promotes Repair and Regeneration after Peripheral Nerve Injury.Applied biochemistry and biotechnology · 2026Article
- Sphingolipid-Neuroinflammation Axis in Parkinson's Disease: Focus on S1P/SPHK1-NF‑κB Signaling.Journal of inflammation research · 2026Review
- Research on the Application of Mesenchymal Stem Cells for Addressing Mitochondrial Damage in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2025Review
- Unveiling the Spatiotemporal dynamics of stress granule phase transition: A key mechanism governing neuronal fate in acute ischemic stroke.Molecular biology reports · 2025Review
- Targeting ER stress in skeletal muscle through physical activity: a strategy for combating neurodegeneration-associated muscle decline.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Parkinson's disease (PD), a prevalent neurodegenerative disorder, demonstrates the critical involvement of endoplasmic reticulum stress (ERS) in its pathogenesis. This review comprehensively examines the role and molecular mechanisms of ERS in PD. ERS represents a cellular stress response triggered by imbalances in endoplasmic reticulum (ER) homeostasis, induced by factors such as hypoxia and misfolded protein aggregation, which activate the unfolded protein response (UPR) through the inositol-requiring enzyme 1 (IRE1), protein kinase R-like endoplasmic reticulum kinase (PERK), and activating transcription factor 6 (ATF6) pathways. Clinical, animal model, and cellular studies have consistently demonstrated a strong association between PD and ERS. Abnormal expression of ERS-related molecules in PD patients' brains and cerebrospinal fluid (CSF) correlates with disease progression. In animal models (e.g., Drosophila and mice), ERS inhibition alleviates dopaminergic neuronal damage. Cellular experiments reveal that PD-mimicking pathological conditions induce ERS, while interactions between ERS and mitochondrial dysfunction promote neuronal apoptosis. Mechanistically, (1) pathological aggregation of α-synuclein (α-syn) and ERS mutually reinforce dopaminergic neuron damage; (2) leucine-rich repeat kinase 2 (LRRK2) gene mutations induce ERS through thrombospondin-1 (THBS1)/transforming growth factor beta 1 (TGF-β1) interactions; (3) molecules such as Parkin and PTEN-induced kinase 1 (PINK1) regulate ERS in PD. Furthermore, ERS interacts with mitochondrial dysfunction, oxidative stress, and neuroinflammation to exacerbate neuronal injury. Emerging therapeutic strategies show significant potential, including artificial intelligence (AI)-assisted drug design targeting ERS pathways and precision medicine approaches exploring non-pharmacological interventions such as personalized electroacupuncture. Future research should focus on elucidating ERS-related mechanisms and identifying novel therapeutic targets to develop more effective treatments for PD patients, ultimately improving their quality of life.
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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.