ArticleFrontiers in immunology2024
Angiotensin type-1 receptor autoantibodies promote alpha-synuclein aggregation in dopaminergic neurons.
Article 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 5 papers.
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Who cites it
5 citing papers in PubMed.
- Targeting GPCR Signaling in Parkinson's Disease: From Molecular Pathology to Exercise-Based Therapeutics.Molecular neurobiology · 2026Review
- Neuroprotective effects of telmisartan in a harmaline-induced model of essential tremor: modulation of the renin-angiotensin system and inflammatory pathways.Frontiers in pharmacology · 2026Article
- Brain-derived extracellular vesicle proteomics reveals neuroprotection induced by the ARB candesartan in Parkinson's disease patients.NPJ Parkinson's disease · 2025Article
- Renin-Angiotensin System Autoantibody Network in Parkinson's Disease Patients.Antioxidants (Basel, Switzerland) · 2025Article
- Serum angiotensin type-1 receptor autoantibodies and neurofilament light chain as markers of neuroaxonal damage in post-COVID patients.Frontiers in immunology · 2025Article
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Authors and funding
4 authors.
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Abstract
Angiotensin, through its type-1 receptor (AT1), is a major inducer of inflammation and oxidative stress, contributing to several diseases. Autoimmune processes have been involved in neurodegeneration, including Parkinson's disease (PD). AT1 autoantibodies (AT1-AA) enhance neurodegeneration and PD, which was related to increased neuronal oxidative stress and neuroinflammation. However, the effect of AT1-AA on α-synuclein aggregation, a major factor in PD progression, has not been studied. In cultures of dopaminergic neurons, we observed that AT1-AA promote aggregation of α-synuclein, as AT1-AA upregulated major mechanisms involved in the α-synuclein aggregation process such as NADPH-oxidase activation and intracellular calcium raising. The results further support the role of AT1 receptors in dopaminergic neuron degeneration, and several recent clinical studies observing the neuroprotective effects of AT1 receptor blockers.
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