ArticleRedox biology2018
A reciprocal relationship between reactive oxygen species and mitochondrial dynamics in neurodegeneration.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.
- Relationship between acute glucose variability and cognitive decline in type 2 diabetes: A systematic review and meta-analysis.PloS one · 2023Pooled it
- Vancomycin disrupts mitochondrial morphology and function and impairs macrophage fungal killing.mBio · 2026Article
- Biochemical Mechanisms of Cellular Stress Adaptation in the Pathogenesis of Chronic Diseases.Molecules (Basel, Switzerland) · 2026Review
- The iron-energy metabolism axis in Alzheimer's pathogenesis: from mechanisms to interventions.Cell death discovery · 2026Review
- The effect of mitoTEMPO on the development of hypoxia-induced pulmonary hypertension in male mice.Physiological reports · 2026Article
- Disruption of neutrophil homeostasis is associated with functional alterations in mitochondria of critically ill COVID-19 patients.Scientific reports · 2026Article
- Scavenging of reactive oxygen and nitrogen species using nanoparticles and their applications in disease management.RSC advances · 2025Review
- Osteogenesis Imperfecta: A Look into the Cerebellum of the Brtl Murine Model.Molecular neurobiology · 2025Article
- The absence of Parkin in hTau mice leads to synaptic mitochondrial dysfunction, alterations to the synaptic proteome, and increased phosphorylated tau in the Hippocampus.Neurobiology of disease · 2025Article
- Oxidative Stress: Pathological Driver in Chronic Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Metabolic reprogramming driven by Ant2 deficiency augments T Cell function and anti-tumor immunity in mice.Nature communications · 2025Article
- The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025Review
- Dietary supplementation and the role of phytochemicals against the Alzheimer's disease: Focus on polyphenolic compounds.The journal of prevention of Alzheimer's disease · 2025Review
- NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Overexpression of mitochondrial fission or mitochondrial fusion genes enhances resilience and extends longevity.Aging cell · 2024Article
- Emerging Functional Connections Between Metabolism and Epigenetic Remodeling in Neural Differentiation.Molecular neurobiology · 2024Review
- Toxic Features and Metabolomic Intervention of Glabrene, an Impurity Found in the Pharmaceutical Product of Glabridin.International journal of molecular sciences · 2024Article
- Detection of a Mitochondrial Fragmentation and Integrated Stress Response Using the Cell Painting Assay.Journal of medicinal chemistry · 2024Article
- Article
- Manipulating mitochondrial reactive oxygen species alters survival in unexpected ways in a Drosophila Cdk5 model of neurodegeneration.Biology open · 2024Article
20 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
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial fragmentation due to fission/fusion imbalance has often been linked to mitochondrial dysfunction and apoptosis in neurodegeneration. Conventionally, it is believed that once mitochondrial morphology shifts away from its physiological tubular form, mitochondria become defective and downstream apoptotic signaling pathways are triggered. However, our study shows that beta-amyloid (Aβ) induces morphological changes in mitochondria where they become granular-shaped and are distinct from fragmented mitochondria in terms of both morphology and functions. Accumulation of mitochondrial reactive oxygen species triggers granular mitochondria formation, while mitoTEMPO (a mitochondria-targeted superoxide scavenger) restores tubular mitochondrial morphology within Aβ-treated neurons. Interestingly, modulations of mitochondria fission and fusion by genetic and pharmacological tools attenuated not only the induction of granular mitochondria, but also mitochondrial superoxide levels in Aβ-treated neurons. Our study shows a reciprocal relationship between mitochondrial dynamics and reactive oxygen species and provides a new potential therapeutic target at early stages of neurodegenerative disease pathogenesis.
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What OpenQuestion holds
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.