[Lead exposure aggravates Aβ1-42-induced microglial activation through mitochondrial calcium uniporter-mediated mitochondrial calcium accumulation].
Year: 2026
Type: article
Abstract: OBJECTIVES: To investigate the role of mitochondrial calcium uniporter (MCU) in lead (Pb)‑potentiated microglial activation induced by amyloid β‑protein (1-42) (Aβ1-42) and the regulatory mechanism by which Pb exacerbates Alzheimer disease (AD)-like pathology. METHODS: +Pb group) were examined for changes in intracellular calcium levels using ICP-MS. Morphological changes of the treated cells were observed, and iNOS release and oxidative stress were assessed with immunofluorescence staining. The changes in cellular MCU protein expression was determined with Western blotting, and cell viability was evaluated using CCK-8 assay. RESULTS: +Pb group, and obviously lowered oxidative stress level, mitochondrial calcium overload, and membrane potential level in the cells. CONCLUSIONS: -activated microglia through upregulation of MCU expression, which causes mitochondrial calcium accumulation to trigger oxidative stress.
Source: PubMed Central
Institutions: Southern Medical University, Air Force Medical University
Language: Chinese
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7223821620