How Chronic Stress Accelerates Biological Aging Through Physiological and Cellular Mechanisms
DOI:
https://doi.org/10.58445/rars.4148Keywords:
chronic stress, biological aging, telomere shortening, oxidative stress, mitochondrial dysfunction, cellular senescence, chronic inflammation, epigenetic aging, stem cell dysfunctionAbstract
Chronic stress is more than a persistent anxiety or exhaustion; its effects extend deep within the body, disrupting physiological and cellular processes over time. While individuals initially experience acute stress as a temporary, short-term response to challenging situations, persistent hardship and adversity can prolong and contribute to the development of chronic stress. Beyond its psychological effects, chronic stress is increasingly recognized as a key agonist in accelerating biological aging in humans. This literature review seeks to examine the underlying physiological and cellular mechanisms contributing to this process, including telomere shortening, oxidative stress, mitochondrial dysfunction, cellular senescence, impaired neural stem cell function, chronic inflammation, and epigenetic aging associated with prolonged stress. Current research suggests that chronic stress can significantly disrupt multiple physiological systems, leading to a rapid decline in biological function and increased susceptibility to aging-related diseases. Collectively, these mechanisms interact and contribute to accelerated biological aging. Understanding these mechanisms may contribute to increasing public awareness of the long-term consequences of chronic stress and provide a strong foundation for future research aimed at preventing biological aging due to chronic stress.
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