ArticleNeurotoxicity research2020
HMGB1 Mediates Paraquat-Induced Neuroinflammatory Responses via Activating RAGE Signaling Pathway.
Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- The Role of High Mobility Group Box 1 (HMGB1) in Neurodegeneration: A Systematic Review.Current neuropharmacology · 2022Pooled it
- Pre-clinical Studies Identifying Molecular Pathways of Neuroinflammation in Parkinson's Disease: A Systematic Review.Frontiers in aging neuroscience · 2022Pooled it
- HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- HMGB1 functional plasticity in neurodegenerative diseases and its translational implications.Frontiers in immunology · 2026Review
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- Pathophysiological role of high mobility group box-1 signaling in neurodegenerative diseases.Inflammopharmacology · 2025Review
- What Can Inflammation Tell Us about Therapeutic Strategies for Parkinson's Disease?International journal of molecular sciences · 2024Review
- Pesticide-Induced Inflammation at a Glance.Toxics · 2023Review
- Calycosin attenuates the inflammatory damage of microglia induced by oxygen and glucose deprivation through the HMGB1/TLR4/NF-κB signaling pathway.Acta biochimica et biophysica Sinica · 2023Article
- Novel therapeutic targets to halt the progression of Parkinson's disease: an in-depth review on molecular signalling cascades.3 Biotech · 2023Review
- Integrin Mac1 mediates paraquat and maneb-induced learning and memory impairments in mice through NADPH oxidase-NLRP3 inflammasome axis-dependent microglial activation.Journal of neuroinflammation · 2023Article
- Review
- Correlation of HMGB1, PON-1, MCP-1, and PeriodontalJournal of healthcare engineering · 2022Article
- Building a Network of Adverse Outcome Pathways (AOPs) Incorporating the Tau-Driven AOP Toward Memory Loss (AOP429).Journal of Alzheimer's disease reports · 2022Review
- Ferritinophagy-Mediated Ferroptosis Involved in Paraquat-Induced Neurotoxicity of Dopaminergic Neurons: Implication for Neurotoxicity in PD.Oxidative medicine and cellular longevity · 2021Article
- HMGB1 Promotes the Release of Sonic Hedgehog From Astrocytes.Frontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Paraquat (PQ), a widely characterized neurotoxicant, has been generally accepted as one of the environmental factors in the etiology of Parkinson's disease (PD). Despite the direct evidence that PQ could induce inflammatory responses in central nervous system, the putative adverse effects of PQ on the neuroimmune interactions have rarely been investigated. High-mobility group box 1 (HMGB1) has been proven to be relevant to the neuroinflammation involved in PD; however, whether and how HMGB1 exerts modulatory effects in nervous system upon PQ exposure remain elusive. Therefore, the present study investigated the underlying association between HMGB1 and PQ exposure in SH-SY5Y cells, which is a well-established in vitro model for PD research. We observed that HMGB1 was markedly increased in a concentration and time-dependent manner upon PQ exposure, and the elevated HMGB1 could be translocated into cytosol and then released to the extracellular milieu of SH-SY5Y cells. Knockdown of HMGB1 inhibited the activation of RAGE-P38-NF-κB signaling pathway and the expression of inflammation cytokines such as TNF-α and IL-6. These results suggested that HMGB1 is involved in the PQ-induced neuron death via activating RAGE signaling pathways and promoting neuroinflammatory responses.
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What OpenQuestion holds
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.