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View article: Organic cation transporter 3 on neuronal mitochondria mediates MPP+-induced mitochondrial dysfunction and neurotoxicity in a TIMM22-dependent manner
Organic cation transporter 3 on neuronal mitochondria mediates MPP+-induced mitochondrial dysfunction and neurotoxicity in a TIMM22-dependent manner Open
Here we found that OCT3 on neuronal mitochondria serves as an effective MPP+ transporter, crucial for mitochondrial MPP+ uptake and MPP+-induced neurotoxicity. Furthermore, TIMM22 downregulation can selectively reduce mitochondrial OCT3 an…
View article: Organic cation transporter 3 on neuronal mitochondria mediates MPP + -induced mitochondrial dysfunction and neurotoxicity in a TIMM22-dependent manner
Organic cation transporter 3 on neuronal mitochondria mediates MPP + -induced mitochondrial dysfunction and neurotoxicity in a TIMM22-dependent manner Open
Background Emerging evidence demonstrates the multifaceted roles of mitochondria in cellular metabolism. The intracellular compartmentalization of metabolites profoundly impacts mitochondrial function and the pathophysiology in many diseas…
View article: WITHDRAWN: Mitochondrial accumulation induced axon dysfunction promotes paranode instability and demyelination in hypoxic-ischemic forms of demyelination
WITHDRAWN: Mitochondrial accumulation induced axon dysfunction promotes paranode instability and demyelination in hypoxic-ischemic forms of demyelination Open
The full text of this preprint has been withdrawn by the authors due to author disagreement with the posting of the preprint. Therefore, the authors do not wish this work to be cited as a reference. Questions should be directed to the corr…
View article: Role of OCT3 and DRP1 in the Transport of Paraquat in Astrocytes: A Mouse Study
Role of OCT3 and DRP1 in the Transport of Paraquat in Astrocytes: A Mouse Study Open
The present study mainly focused on the transport mechanisms of PQ between the dopaminergic neurons and astrocytes. Lower OCT3 levels were found in the older or chronically PQ-treated mice. Astrocytes with DRP1 inhibition (by viral tools o…
View article: Dl-3-n-Butylphthalide Alleviates Demyelination and Improves Cognitive Function by Promoting Mitochondrial Dynamics in White Matter Lesions
Dl-3-n-Butylphthalide Alleviates Demyelination and Improves Cognitive Function by Promoting Mitochondrial Dynamics in White Matter Lesions Open
White matter lesions (WMLs) are a type of cerebrovascular disorder accompanied by demyelination and cognitive decline. Dl-3-n-butylphthalide (D1-NBP) is a neuroprotective drug used for the treatment of ischemic cerebrovascular diseases, al…
View article: Mesenchymal-Stem-Cell–Derived Extracellular Vesicles Mitigate Trained Immunity in the Brain
Mesenchymal-Stem-Cell–Derived Extracellular Vesicles Mitigate Trained Immunity in the Brain Open
Trained immunity was recently discovered in innate immune cells and shown to facilitate the clearance of pathogens at the time of occurrence of the second insult. However, it exacerbates several aspects of neuropathologies, and proper ther…
View article: WITHDRAWN: Mitochondrial accumulation induced axon dysfunction promotes paranode instability and demyelination in hypoxic-ischemic forms of demyelination
WITHDRAWN: Mitochondrial accumulation induced axon dysfunction promotes paranode instability and demyelination in hypoxic-ischemic forms of demyelination Open
Hypoxic-ischemic forms of demyelination, caused by chronic or acute reduction of blood flow in subcortical white matter, is increasingly considered as an important contributor to cognitive decline. However, it remains unclear how hypoxia/i…
View article: The <i>FAM171A2</i> gene is a key regulator of progranulin expression and modifies the risk of multiple neurodegenerative diseases
The <i>FAM171A2</i> gene is a key regulator of progranulin expression and modifies the risk of multiple neurodegenerative diseases Open
The FAM171A2 gene is a key regulator of progranulin expression and modifies the risk of multiple neurodegenerative diseases.
View article: Microglial exosomes facilitate α-synuclein transmission in Parkinson’s disease
Microglial exosomes facilitate α-synuclein transmission in Parkinson’s disease Open
Accumulation of neuronal α-synuclein is a prominent feature in Parkinson’s disease. More recently, such abnormal protein aggregation has been reported to spread from cell to cell and exosomes are considered as important mediators. The focu…