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Effects of fine particulate matter on neuroblastoma cell line: metabolic and lipid deregulations and their consequences on the onset of neurological diseases

AI Summary
  • PM2.5 exposure induces mitochondrial damage, endoplasmic reticulum stress, oxidative stress, calcium dyshomeostasis and lipid dysregulation in SH-SY5Y neuronal cells.
  • These alterations trigger apoptosis and autophagy dependent ferroptosis, with lipid peroxidation and oxidative damage emerging as central drivers of neuronal degeneration.
  • Translation from in vitro to in vivo and human pathology is limited; defining molecular events is essential to develop therapies preventing pollution related neurodegeneration.
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Biochimie. 2026 Sep 18:S0300-9084(26)00230-0. doi: 10.1016/j.biochi.2026.09.011. Online ahead of print.

ABSTRACT

Particulate Matter (PM) contained in atmospheric pollution can interact with pulmonary, cardiac and nervous systems. Recent studies focus on the impact of PM2.5 on the brain and on their potential role in the onset of neurodegenerative diseases (ND) such as Alzheimer’s disease. Using human neuroblastoma SH-SY5Y cell line as an in vitro neurodegenerative model, multiple interconnected cellular dysfunctions induced by PM2.5 exposure have been highlighted. This includes mitochondrial damages, reticulum endoplasmic stress, oxidative stress, calcium dyshomeostasis and lipid dysregulation. These alterations activate multiple cell death pathway though apoptosis and autophagy-dependent ferroptosis. This review aims to provide an integrated overview of these mechanisms, to better understand the association between PM2.5 exposure and cell degeneration. A particular attention is given to lipid peroxidation and oxidative damage as emerging drivers of neuronal degeneration. Despite significant advances, important gaps remain regarding the translation of in vitro findings to in vivo models and particularly to human pathology. A better understanding of key molecular events is essential to identify therapeutic targets to mitigate or prevent pollution-related neurodegenerative processes.

PMID:42759687 | DOI:10.1016/j.biochi.2026.09.011

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