ArticleScientific reports2016
NADPH oxidase promotes Parkinsonian phenotypes by impairing autophagic flux in an mTORC1-independent fashion in a cellular model of Parkinson's disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- NADPH oxidases in Parkinson's disease: a systematic review.Molecular neurodegeneration · 2017Pooled it
- Redox-modulation of regulated cell death: implications for synergistic anticancer therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Modulation of Bromo- and Extra-Terminal Domain (BET) Proteins Exerts Neuroprotective Effects in Cell Culture Models of Parkinson's Disease.Biomedicines · 2026Article
- 18β-Glycyrrhetinic Acid Regulates Endoplasmic Reticulum Stress and Autophagy Dysregulation in the MPTP/p-Induced Model of Parkinson Disease.Molecular neurobiology · 2025Article
- p75NTR Modulation by LM11A-31 Counteracts Oxidative Stress and Cholesterol Dysmetabolism in a Rotenone-Induced Cell Model of Parkinson's Disease.Neurochemical research · 2025Article
- Redox homeostasis dysregulation in noise-induced hearing loss: oxidative stress and antioxidant treatment.Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale · 2023Review
- Endoplasmic reticulum stress and unfolded protein accumulation correlate to seizure recurrence in focal cortical dysplasia patients.Cell stress & chaperones · 2022Article
- The Hidden Notes of Redox Balance in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- NADPH oxidase family proteins: signaling dynamics to disease management.Cellular & molecular immunology · 2022Review
- A Novel NOX Inhibitor Treatment Attenuates Parkinson's Disease-Related Pathology in Mouse Models.International journal of molecular sciences · 2022Article
- BMAL1 drives muscle repair through control of hypoxic NADGenes & development · 2022Article
- Building a Network of Adverse Outcome Pathways (AOPs) Incorporating the Tau-Driven AOP Toward Memory Loss (AOP429).Journal of Alzheimer's disease reports · 2022Review
- Fluorescent Protein-Based Autophagy Biosensors.Materials (Basel, Switzerland) · 2021Review
- Vulnerability of subcellular structures to pathogenesis induced by rotenone in SH-SY5Y cells.Physiological research · 2021Article
- Variants inBrain communications · 2021Article
- Diclofenac impairs autophagic flux via oxidative stress and lysosomal dysfunction: Implications for hepatotoxicity.Redox biology · 2020Article
- Lysosomal quality control of cell fate: a novel therapeutic target for human diseases.Cell death & disease · 2020Review
- The emerging roles of vacuolar-type ATPase-dependent Lysosomal acidification in neurodegenerative diseases.Translational neurodegeneration · 2020Review
- Autophagy Function and Regulation in Kidney Disease.Biomolecules · 2020Review
- Pretreatment of Ascorbic Acid Inhibits MPTP-Induced Astrocytic Oxidative Stress through Suppressing NF-Neural plasticity · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress and aberrant accumulation of misfolded proteins in the cytosol are key pathological features associated with Parkinson's disease (PD). NADPH oxidase (Nox2) is upregulated in the pathogenesis of PD; however, the underlying mechanism(s) of Nox2-mediated oxidative stress in PD pathogenesis are still unknown. Using a rotenone-inducible cellular model of PD, we observed that a short exposure to rotenone (0.5 μM) resulted in impaired autophagic flux through activation of a Nox2 dependent Src/PI3K/Akt axis, with a consequent disruption of a Beclin1-VPS34 interaction that was independent of mTORC1 activity. Sustained exposure to rotenone at a higher dose (10 μM) decreased mTORC1 activity; however, autophagic flux was still impaired due to dysregulation of lysosomal activity with subsequent induction of the apoptotic machinery. Cumulatively, our results highlight a complex pathogenic mechanism for PD where short- and long-term oxidative stress alters different signaling pathways, ultimately resulting in anomalous autophagic activity and disease phenotype. Inhibition of Nox2-dependent oxidative stress attenuated the impaired autophagy and cell death, highlighting the importance and therapeutic potential of these pathways for treating patients with PD.
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