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This mitochondrial dysfunction-induced immunosenescence promotes premature aging phenotypes and multimorbidity, creating a pro-inflammatory environment that simultaneously accelerates atherosclerosis progression and neuroinflammation

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In vivo studies in ApoE / mice show that chronic oral PS-NP exposure accelerates atherosclerotic plaque formation via increased smooth muscle cell migration regulated by kinesin family member 15 (KIF15) [101]