The AMPK-PGC-1α-SIRT3 axis mediates mitochondrial metabolic dysfunction and neuronal senescence induced by Al(mal)

Huifang Zhang, Xinrong Gao, Zhaoya Jin, Yang Liu, Jinzhu Yin, Rui Zhang

Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan, China; MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention in Shanxi, Taiyuan, China. Electronic address: [email protected] of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan, China; MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention in Shanxi, Taiyuan, China. Electronic address: [email protected]. · pubmed

Paper

Abstract

Aluminum (Al) is a widely distributed environmental metal whose chronic exposure has been implicated in neurotoxicity and increased risk of neurodegenerative disorders. However, the molecular mechanisms linking aluminum exposure to neuronal metabolic dysfunction and senescence remain incompletely understood. In this study, mouse hippocampal neuronal HT22 cells were exposed to aluminum maltolate [Al(mal)

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Research summary

The paper claims that the AMPK-PGC-1α-SIRT3 axis mediates mitochondrial metabolic dysfunction and neuronal senescence induced by aluminum exposure. This research is relevant as it explores the molecular mechanisms of neuronal senescence, which is a key aspect of aging and age-related diseases.

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