ArticleNeurotoxicity research2022
Paraquat Inhibits Autophagy Via Intensifying the Interaction Between HMGB1 and α-Synuclein.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Interrelationship between PQ exposure and Parkinson disease: A systematic review and meta-analysis.Medicine · 2025Pooled it
- High mobility group box 1 and its post-translational modifications: Molecular mechanisms underlying neurodegenerative disease pathogenesis.Neural regeneration research · 2026Article
- Article
- Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson's Disease with Potential Therapeutic Implications.Biomolecules · 2025Review
- MicroRNA-124-3p Modulates Alpha-Synuclein Expression Levels in a Paraquat-Induced in vivo Model for Parkinson's Disease.Neurochemical research · 2024Article
- High Mobility Group Box 1 Protein: A Plausible Therapeutic Molecular Target in Parkinson's Disease.Current pharmaceutical biotechnology · 2024Review
- Pesticide-Induced Inflammation at a Glance.Toxics · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Paraquat, a widely used herbicide, is associated with an increased risk of Parkinson's disease (PD). PQ induces upregulation and accumulation of α-synuclein in neurons, which is one of the major pathological hallmarks of PD. Autophagy, as the major mechanism for the clearance of α-synuclein, is disrupted upon pesticide exposure as well as in PD patients. Meanwhile, HMGB1 is involved in autophagy dysfunction and particularly relevant to PD. However, whether PQ exposure affects HMGB1, α-synuclein, and autophagy function have rarely been reported. In this study, we found that PQ exposure impaired autophagy function via disturbing the complex formation of HMGB1 and Beclin1. Moreover, the expression of α-synuclein is modulated by HMGB1 and the interaction between HMGB1 and α-synuclein was intensified by PQ exposure. Taken together, our results revealed that HMGB1-mediated α-synuclein accumulation could competitively perturb the complex formation of HMGB1 and Beclin1, thereby inhibiting the autophagy function in SH-SY5Y cells.
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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.