ArticleCNS neuroscience & therapeutics2025
The Role of P62/Nrf2/Keap1 Signaling Pathway in Lead-Induced Neurological Dysfunction.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Fermentation Status Dictates Organ-Selective Protection of a Millet-Based Dairy Beverage Against Sub-Chronic Lead Toxicity in Rats.Biological trace element research · 2026Article
- The Protective Effect of Naringenin against Lead-Induced Hepatotoxicity in Rats: Mechanisms Involving Oxidative Stress Mitigation, Activation of PINK1/Parkin and Nrf2/NQO1 Pathways, and Autophagy Induction.Biological trace element research · 2026Article
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Influence of Extraction Method on the Bioactivity ofFoods (Basel, Switzerland) · 2026Article
- Ferroptosis in multiple myeloma: molecular mechanisms and therapeutic opportunities.Frontiers in oncology · 2026Review
- The Role of P62/Nrf2/Keap1 Signaling Pathway in Lead-Induced Neurological Dysfunction.CNS neuroscience & therapeutics · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundLead (Pb) exposure is recognized for its contribution to the development of neurodegenerative diseases. However, the precise mechanisms underlying Pb-induced neurological dysfunction remain elusive. This study aimed to investigate the role of oxidative stress and the autophagy-related P62/kelch like ECH-associated protein 1 (Keap1)/Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in neuronal impairment caused by Pb.
methodsBy employing both in vivo and in vitro approaches, we explored the involvement of the P62/Nrf2/Keap1 pathway in Pb-induced neurotoxicity.
resultsOur findings demonstrated that Pb exposure triggers excessive production of reactive oxygen species (ROS), upregulates Keap1 protein expressions, promotes Nrf2 degradation, and inhibits expression of antioxidant proteins such as heme Oxygenase-1 (HO-1) and glutathione peroxidase (GPx), resulting in oxidative damage in neurons. Furthermore, we observed that the autophagy protein P62 disrupts the normal autophagy process by interacting with the Nrf2/Keap1 axis, leading to an accumulation of Tau, a protein associated with Alzheimer's disease (AD), ultimately resulting in neurodegeneration. However, treatment with the antioxidant N-acetylcysteine, Nrf2 activator Artemisitene, and autophagy activator Rapamycin attenuated these detrimental changes.
conclusionThe P62/Nrf2/Keap1 pathway mediates Pb-induced neuronal dysfunction and highlights its potential as a therapeutic target for mitigating the neurodegenerative effects associated with Pb exposure.
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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 Socratic graph.