Stress Hormones: Unveiling the Role in Accelerated Cellular Senescence

Area of Science:

• Cellular and Molecular Biology
• Gerontology
• Endocrinology

Background:

• Cellular senescence, a state of irreversible growth arrest, is influenced by genetics, environment, and behavior.
• Emerging evidence highlights stress as a significant inducer of cellular senescence, contributing to accelerated aging.
• Stress impacts cellular function and structure via neuroendocrine pathways, leading to premature aging.

Purpose of the Study:

• To review the mechanisms of stress-induced cellular senescence.
• To explore the role of stress hormones in this process.
• To discuss therapeutic targets and pharmacological interventions for stress-induced premature senescence.

Main Methods:

• Literature review integrating recent research on stress-induced cellular senescence.
• Analysis of molecular pathways linking stress to senescence.
• Evaluation of therapeutic strategies and pharmacological agents.

Main Results:

• Stress activates the hypothalamus-pituitary-adrenal and sympathetic adrenal medullary axes, releasing cortisol and catecholamines.
• These hormones induce mitochondrial dysfunction, oxidative stress, DNA damage, and inflammation, accelerating senescence.
• Stress-induced cellular senescence is linked to age-related macular degeneration, chronic kidney disease, type 2 diabetes, cardiovascular disease, and obstructive sleep apnea.

Conclusions:

• Stress is a critical factor in cellular senescence, mediated by hormonal responses.
• Understanding these mechanisms offers potential therapeutic avenues for stress-related chronic diseases.
• Further research is needed to optimize pharmacological interventions for stress-induced premature senescence.