ReviewFrontiers in immunology2024
Mitophagy-associated programmed neuronal death and neuroinflammation.
Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed.
- Revisiting Alzheimer's Disease Through the Somatostatin-Mitochondria Axis.Molecular neurobiology · 2026Review
- Lipid metabolism and neurodegeneration: Mechanistic insights and therapeutic targets.Ageing research reviews · 2026Review
- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- Physical Exercise Counteracts Impaired Cognition by Improving Mitochondrial Function.International journal of molecular sciences · 2026Review
- MG132-mediated inhibition of rabies virus replication via the Nrf2/SQSTM1/PINK1/Parkin autophagy pathway.Virology journal · 2026Article
- Mitochondrial dysfunction in sleep deprivation.Metabolic brain disease · 2026Review
- Roles of mitophagy and immune infiltration in Parkinson's disease: new perspectives from bioinformatics analysis and A53T transgenic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Ferroptosis and Cuproptosis in Cancer and Neurodegeneration: A Comprehensive Review of Modulation by Iron and Copper Chelators and Related Agents.Biomolecules · 2026Review
- Article
- Mitochondria-Associated MicroRNAs: Emerging Roles in the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- Review
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- Neuroimaging evidence of mitochondrial dysfunction and inflammation in psychiatric disorders: a review.Psychoradiology · 2026Review
- Urapidil as a neuroprotective agent: targeting hypoxia, inflammation, and oxidative stress in traumatic brain injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Alterations ofCurrent Alzheimer research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are crucial organelles that play a central role in cellular metabolism and programmed cell death in eukaryotic cells. Mitochondrial autophagy (mitophagy) is a selective process where damaged mitochondria are encapsulated and degraded through autophagic mechanisms, ensuring the maintenance of both mitochondrial and cellular homeostasis. Excessive programmed cell death in neurons can result in functional impairments following cerebral ischemia and trauma, as well as in chronic neurodegenerative diseases, leading to irreversible declines in motor and cognitive functions. Neuroinflammation, an inflammatory response of the central nervous system to factors disrupting homeostasis, is a common feature across various neurological events, including ischemic, infectious, traumatic, and neurodegenerative conditions. Emerging research suggests that regulating autophagy may offer a promising therapeutic avenue for treating certain neurological diseases. Furthermore, existing literature indicates that various small molecule autophagy regulators have been tested in animal models and are linked to neurological disease outcomes. This review explores the role of mitophagy in programmed neuronal death and its connection to neuroinflammation.
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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.