ReviewMolecular neurobiology2010
Redox reactions induced by nitrosative stress mediate protein misfolding and mitochondrial dysfunction in neurodegenerative diseases.
Review in Molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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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.
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Who cites it
69 citing papers in PubMed, 149 citations in OpenAlex.
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- Interplay Between Aging and Tau Pathology in Alzheimer's Disease: Mechanisms and Translational Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Investigating antioxidant effects of hamamelitannin-conjugated zinc oxide nanoparticles on oxidative stress-Induced neurotoxicity in zebrafish larvae model.Molecular biology reports · 2024Article
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- Mitochondrial proteome research: the road ahead.Nature reviews. Molecular cell biology · 2024Review
- The Drp1-Mediated Mitochondrial Fission Protein Interactome as an Emerging Core Player in Mitochondrial Dynamics and Cardiovascular Disease Therapy.International journal of molecular sciences · 2023Review
- Oxidative Stress in Long-Term Exposure to Multi-Walled Carbon Nanotubes in Male Rats.Antioxidants (Basel, Switzerland) · 2023Article
- Triose-phosphate isomerase deficiency is associated with a dysregulation of synaptic vesicle recycling inFrontiers in synaptic neuroscience · 2023Article
- S-Glutathionylation and S-Nitrosylation in Mitochondria: Focus on Homeostasis and Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Mechanisms and pathophysiology of Barrett oesophagus.Nature reviews. Gastroenterology & hepatology · 2022Review
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- The modulatory effect of taurine on benzo (a) pyrene-induced hepatorenal toxicity.Toxicology research · 2021Article
- Sildenafil Alleviates Murine Experimental Autoimmune Encephalomyelitis by Triggering Autophagy in the Spinal Cord.Frontiers in immunology · 2021Article
- Chromon-3-aldehyde derivatives restore mitochondrial function in rat cerebral ischemia.Iranian journal of basic medical sciences · 2020Article
- Design of Light-Sensitive Triggers for Endothelial NO-Synthase Activation.Antioxidants (Basel, Switzerland) · 2020Article
- Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson's Disease Models.International journal of molecular sciences · 2019Review
- Sp1-regulated expression of p11 contributes to motor neuron degeneration by membrane insertion of TASK1.Nature communications · 2019Article
- Tauopathy: A common mechanism for neurodegeneration and brain aging.Mechanisms of ageing and development · 2019Review
9 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
Abstract
Overstimulation of N-methyl-D-aspartate (NMDA)-type glutamate receptors accounts, at least in part, for excitotoxic neuronal damage, potentially contributing to a wide range of acute and chronic neurologic diseases. Neurodegenerative disorders including Alzheimer's disease (AD) and Parkinson's disease (PD), manifest deposits of misfolded or aggregated proteins, and result from synaptic injury and neuronal death. Recent studies have suggested that nitrosative stress due to generation of excessive nitric oxide (NO) can mediate excitotoxicity in part by triggering protein misfolding and aggregation, and mitochondrial fragmentation in the absence of genetic predisposition. S-Nitrosylation, or covalent reaction of NO with specific protein thiol groups, represents a convergent signal pathway contributing to NO-induced protein misfolding and aggregation, compromised dynamics of mitochondrial fission-fusion process, thus leading to neurotoxicity. Here, we review the effect of S-nitrosylation on protein function under excitotoxic conditions, and present evidence suggesting that NO contributes to protein misfolding and aggregation via S-nitrosylating protein-disulfide isomerase or the E3 ubiquitin ligase parkin, and mitochondrial fragmentation through beta-amyloid-related S-nitrosylation of dynamin-related protein-1. Moreover, we also discuss that inhibition of excessive NMDA receptor activity by memantine, an uncompetitive/fast off-rate (UFO) drug can ameliorate excessive production of NO, protein misfolding and aggregation, mitochondrial fragmentation, and neurodegeneration.
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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.