ReviewFrontiers in aging neuroscience2021
The Cross-Links of Endoplasmic Reticulum Stress, Autophagy, and Neurodegeneration in Parkinson's Disease.
Review in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 93 citations in OpenAlex.
- Ginsenoside Rg1, a Natural Lysosomal Enhancer, Alleviates Parkinson's Disease Pathology via Cathepsin D-Dependent Regulation of α-Synuclein Homeostasis.Phytotherapy research : PTR · 2026Article
- Article
- Network Biology of Alzheimer's Disease and Related Neurodegenerative Disorders: Molecular Mechanisms and Therapeutic Strategies.Biomolecules · 2026Review
- In silico analysis of PERK interactions with engineered alpha lactalbumin peptides using molecular dynamics simulations.Scientific reports · 2026Article
- ABCG2-autophagy regulatory axis in cancer stem cells: implication in cancer metastasis, recurrence and chemotherapy resistance.Cell communication and signaling : CCS · 2026Review
- Molecular Pathogenesis of Memory Impairment in Parkinson's Disease: An Exploration of Underlying Mechanisms.Health science reports · 2026Article
- Intricate interplay between ORMDL3, ER stress, and autophagy in the diabetic intestine.Molecular and cellular biochemistry · 2026Article
- Endoplasmic reticulum stress-mediated cell death in spinal cord injury: from molecular mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2026Review
- Leveraging Foundation Models for the Characterization of Small-RNA Properties.Computational and structural biotechnology journal · 2026Article
- Paeony root prevents 6-hydroxydopamine-induced neurotoxicity by regulating autophagic dysfunction via AKT signaling in Parkinson's disease models.Metabolic brain disease · 2025Article
- Multi-Omics Analysis Reveals Distinct Lipid Remodelling and Mitochondrial Stress in SH-SY5Y Cells Modelling Parkinson's Disease.Metabolites · 2025Article
- 18β-Glycyrrhetinic Acid Regulates Endoplasmic Reticulum Stress and Autophagy Dysregulation in the MPTP/p-Induced Model of Parkinson Disease.Molecular neurobiology · 2025Article
- Astaxanthin-Loaded Silver Nanoparticles Mitigate 6-OHDA-Induced Parkinson's via ER Stress and PI3K/Akt/mTOR Signaling.Molecular neurobiology · 2025Article
- Inhibition of PDE4 Alleviates Endoplasmic Reticulum Stress and Neuronal Damage via Activation of Nrf2/HO-1 in Parkinson's Disease.Molecular neurobiology · 2025Article
- Role of Fibroblast Growth Factors in Neurological Disorders: Insight into Therapeutic Approaches and Molecular Mechanisms.Molecular neurobiology · 2025Review
- The Neuroprotective Effects of the Crinoid Natural Compound Rhodoptilometrin in Parkinson's Disease Experimental Models: Implications for ER Stress and Autophagy Modulation.ACS chemical neuroscience · 2025Article
- Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.CNS neuroscience & therapeutics · 2025Review
- Neuroprotective Effects of Morin Against Cadmium- and Arsenic-Induced Cell Damage in PC12 Neurons.Biological trace element research · 2025Article
- Endurance Training Alleviates Metabolic-Associated Fatty-Liver Disease (MAFLD)-Related Testicular Impairments via Endoplasmic Reticulum Stress Regulation.Journal of clinical laboratory analysis · 2025Article
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is the most common neurodegenerative movement disorder, and it is characterized by the selective loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc), as well as the presence of intracellular inclusions with α-synuclein as the main component in surviving DA neurons. Emerging evidence suggests that the imbalance of proteostasis is a key pathogenic factor for PD. Endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and autophagy, two major pathways for maintaining proteostasis, play important roles in PD pathology and are considered as attractive therapeutic targets for PD treatment. However, although ER stress/UPR and autophagy appear to be independent cellular processes, they are closely related to each other. In this review, we focused on the roles and molecular cross-links between ER stress/UPR and autophagy in PD pathology. We systematically reviewed and summarized the most recent advances in regulation of ER stress/UPR and autophagy, and their cross-linking mechanisms. We also reviewed and discussed the mechanisms of the coexisting ER stress/UPR activation and dysregulated autophagy in the lesion regions of PD patients, and the underlying roles and molecular crosslinks between ER stress/UPR activation and the dysregulated autophagy in DA neurodegeneration induced by PD-associated genetic factors and PD-related neurotoxins. Finally, we indicate that the combined regulation of ER stress/UPR and autophagy would be a more effective treatment for PD rather than regulating one of these conditions alone.
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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.