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Updated: Jan 7, 2026

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
Published on: November 22, 2017
Mitophagy in Age-Dependent Neurodegeneration
V S Sukhorukov1,2, A V Egorova1,2, A S Romanenko1,2
1Russian Center of Neurology and Neurosciences, Moscow, 125367 Russia.
Abstract:
Mitochondrial dysfunction is one of the pathogenetic mechanisms of neuronal damage during aging. The high energy dependence of neurons makes them particularly vulnerable to age-related changes accompanied by oxidative stress and impaired energy metabolism. The maintenance of a pool of functional mitochondria is regulated by mitophagy, which ensures the utilization of damaged organelles, thereby preventing the progression of mitochondrial dysfunction. Brain aging is accompanied by a reduced level of activity of metabolic processes, aggravated mitochondrial dysfunction, and an increased risk of developing neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. This review highlights the molecular and signaling pathways of mitophagy and its dysregulation during physiological and pathological aging, which is of particular interest for identifying pharmaceutical targets and developing potential therapies for neurodegenerative conditions.
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