ArticleCell death discovery2025
Plin4 modulates lipid droplet accumulation and ferroptosis in neurons exposed to benzo[a]pyrene.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- TRPA1 deficiency alters brown adipose tissue proteome and thermogenic gene expression during cold exposure in mice.Biochemistry and biophysics reports · 2026Article
- Multi-regional transcriptomic analysis reveals early nociceptive and neuroinflammatory alterations in APP/PS1 mice.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
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Abstract
Benzo[a]pyrene (B[a]P), an environmental neurotoxin, induces cognitive decline through ferroptosis-mediated mechanisms. Transcriptomic analysis (GSE75206) of B[a]P-exposed mouse hippocampus identified 1668 differentially expressed genes, with Plin4 emerging as a key regulator linked to ferroptosis and lipid droplet (LD) accumulation. Behavioral tests confirmed hippocampal-dependent cognitive impairment and Plin4 upregulation. Molecular analyses demonstrated ferroptosis activation, evidenced by altered expression of related genes (Gpx4, Slc7a11, Ptgs2) and biochemical markers of lipid peroxidation and iron imbalance. In HT22 cells, Benzopyrene-7,8-Diol-9,10-Epoxide (BPDE) dose-dependently elevated Plin4 expression, inducing mitochondrial damage and ferroptosis. Silencing Plin4 reversed BPDE-induced ferroptosis by restoring redox balance, reducing LD accumulation, and improving mitochondrial integrity. Mechanistically, Plin4 amplifies B[a]P neurotoxicity by exacerbating iron overload and LD accumulation, sensitizing neurons to ferroptosis. This study identifies Plin4 as a central mediator of environmental pollutant-induced neurodegeneration and proposes it as a therapeutic target for ferroptosis-related cognitive disorders.
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Registered trials
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