ArticleCell biology and toxicology2025
Manganese exposure induces parkinsonism-like symptoms by Serpina3n-TFEB-v/p-ATPase signaling mediated lysosomal dysfunction.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Neurotoxicity, α-synuclein pathology, and mitochondrial dysfunction: A comparative study of different mouse models of Parkinson's disease.Neural regeneration research · 2026Article
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- The Role of Mitochondrial Quality Control in Manganese-induced Neurotoxicity.Neurotoxicity research · 2025Review
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12 authors.
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Abstract
Manganese (Mn) is a neurotoxin that has been etiologically linked to the development of neurodegenerative diseases in the case of overexposure. It is widely accepted that overexposure to Mn leads to manganism, which has clinical symptoms similar to Parkinson's disease (PD), and is referred to as parkinsonism. Astrocytes have been reported to scavenge and degrade extracellular α-synuclein (α-Syn) in the brain. However, the mechanisms of Mn-induced neurotoxicity associated with PD remain unclear. Serpina3n is highly expressed in astrocytes and has been implicated in several neuropathologies. The role Serpina3n plays in Mn neurotoxicity and PD pathogenesis is still unknown. Here, we used wild-type and Serpina3n knockout (KO) C57BL/6 J mice with i.p. injection of 32.5 mg/kg MnCl
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