Skin aging is a multifactorial biological process driven by the interplay of intrinsic and extrinsic influences. Progressive deterioration of the dermal collagen fiber network represents a central structural hallmark of this process. Both the quantity and functional quality of cutaneous collagen are modified by numerous factors, including autoimmune disease, chronological aging and psychological stress. This narrative review synthesizes current evidence on the neuroendocrine, molecular and cellular pathways through which psychological stress may influence dermal collagen and elastin remodeling, thereby contributing to premature skin aging. Available evidence suggests that chronic activation of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system leads to increased glucocorticoid and catecholamine signaling, oxidative stress, extracellular matrix degradation and impaired epidermal barrier function. Understanding these mechanisms may support the development of integrated therapeutic strategies targeting stress-responsive pathways to preserve skin structure and function. Future studies that track patients over time and examine molecular changes are needed to turn these findings into ways to prevent or treat stress-related skin aging.
Ahmed et al. (Mon,) studied this question.
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