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reported that in 16HBE cells, BRPM2.5 treatment promoted excessive mitochondrial fission by upregulating phosphorylated dynamin-related protein 1 (p-Drp1) protein expression, accompanied by mitochondrial dysfunction, such as increased mtROS production, decreased MMP, and reduced ATP levels, which exacerbated inflammation and increased cell death (Gao et al., 2022)

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