This paper proposes and systematically elaborates on the hypothesis of 'Comprehensive Decoding of Aging Pathways,' which defines mitochondrial dysfunction as the 'primary cause' of aging. Mitochondrial dysfunction is not a passive damage but an active driver that initiates the aging process. It triggers a series of cascade reactions by affecting cellular energy metabolism, redox balance, and signal transduction, including metabolic disorders of sugar and lipids (secondary cause), decline of the GH-IGF-1 axis (tertiary cause), collapse of the antioxidant network (quaternary cause), immune collapse caused by imbalance of the inflammation-glucocorticoid axis (quinary cause), and accumulation and clearance of damaged senescent cells (sixth cause). These factors are interrelated, forming a self-reinforcing locking mechanism that leads to continuous decline in bodily functions. The article also deeply analyzes key regulatory networks, such as interactions between genes and pathways like PPARα, AMPK, PGC-1α, NRF1/NRF2, as well as the roles of blood oxygen supply, vitamin metabolism, and calcium signaling in aging. Based on this model, potential anti-aging strategies are proposed, such as high-protein ketogenic diet, time-restricted fasting, and systemic interventions, aiming to reverse mitochondrial dysfunction from the upstream. Finally, the authors review the theoretical development process, from the initial focus on mTOR to ultimately tracing back to mitochondrial dysfunction, emphasizing the core role of mitochondrial function in anti-aging research.
A Note on the Text:
Please be aware that this paper has been translated from its original language into English with the assistance of AI. While I have strived for accuracy, I am not a native English speaker. Therefore, if you encounter passages that seem logically weak or unclear, it may be due to a loss of nuance or precision in the translation process, rather than a flaw in the underlying theory itself. I welcome any questions for clarification.
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