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Mitochondrial damage associated with apoptosis and necrosis can release damage-associated molecular pattern molecules (DAMPs) and histones that activate inflammatory pathways to exacerbate the lung disease (Koenig and Buskiewicz-Koenig, 2022)

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[97] demonstrated increased oxidative stress, mitochondrial DNA mutations and atherosclerosis in the aortic root of ApoE / mice following exposure to e-cigarettes with 2.4% nicotine