ArticleFrontiers in molecular neuroscience2023
Cardiolipin externalization mediates prion protein (PrP) peptide 106-126-associated mitophagy and mitochondrial dysfunction.
Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Historical rise of cancer and dietary linoleic acid: Mechanisms and therapeutic strategies.World journal of clinical oncology · 2025Review
- DEAD-Box Helicase 6 Blockade in Brain-Derived Aβ Oligomers From Alzheimer's Disease Patients Attenuates Neurotoxicity.MedComm · 2025Article
- Deuterium trafficking, mitochondrial dysfunction, copper homeostasis, and neurodegenerative disease.Frontiers in molecular biosciences · 2025Review
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- The role of mitophagy in metabolic diseases and its exercise intervention.Frontiers in physiology · 2024Review
- Cristae formation is a mechanical buckling event controlled by the inner mitochondrial membrane lipidome.The EMBO journal · 2023Article
- Cristae formation is a mechanical buckling event controlled by the inner membrane lipidome.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper mitochondrial performance is imperative for the maintenance of normal neuronal function to prevent the development of neurodegenerative diseases. Persistent accumulation of damaged mitochondria plays a role in prion disease pathogenesis, which involves a chain of events that culminate in the generation of reactive oxygen species and neuronal death. Our previous studies have demonstrated that PINK1/Parkin-mediated mitophagy induced by PrP
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Registered trials
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