Role of Mitochondrial Autophagy in Cell Aging and Its Molecular Mechanism
DOI:
https://doi.org/10.62051/91sfnw58Keywords:
mitochondrial autophagy; cell senescence; molecular mechanism; PINK1/Parkin.Abstract
Cell aging is the basis of organism aging, which is closely related to many aging-related diseases. Mitochondria, as the energy factory of cells, its function decline and damage play a key role in the process of cell aging. Mitochondrial autophagy is an intracellular quality control mechanism to selectively remove damaged mitochondria, which can delay cell aging by maintaining mitochondrial function and intracellular homeostasis. This paper reviews the role of mitochondrial autophagy in cell aging and its molecular mechanism. Mitochondrial autophagy is closely related to the occurrence of aging-related diseases such as Parkinson's disease (PD), Alzheimer's disease (AD) and heart failure, and activating mitochondrial autophagy can prolong the life of model organisms. The molecular mechanisms of mitochondrial autophagy mainly include ubiquitin-dependent pathway (PINK1/Parkin pathway) and non-ubiquitin-dependent pathway (NIX, BNIP3, FUNDC1-mediated autophagy), and are regulated by AMPK/mTOR, Sirtuin and other signal pathways. In addition, metabolic state and nutritional signals finely regulate the dynamic process of mitochondrial autophagy through energy perception mechanism. Although mitochondrial autophagy shows great potential in delaying aging and treating diseases, its clinical application still faces many challenges. Future research needs to further explore the molecular mechanism of mitochondrial autophagy, develop more accurate intervention methods, and verify its safety and effectiveness through clinical trials, so as to promote the development of anti-aging and disease treatment strategies.
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