JAAD international · 2025
The brain-skin connection: A narrative review of neuroendocrine and immune pathways.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tan Chang Chuen, Soh Krystal Valerie, Wang Eugene, Choi Ellie Ci-En
Аннотация
BACKGROUND: Stress is a well-established trigger for many skin diseases; yet its biological mechanisms are poorly understood.
OBJECTIVE: To synthesize current evidence on brain-skin pathways, emphasizing key mediators and feedback loops that explain how stress exacerbates skin disease and vice versa.
METHODS: A comprehensive search through August 25, 2025, using terms related to brain-skin communication, psychodermatology, and stress-related pathophysiology included both in-vivo and in-vitro animal and human studies.
RESULTS: 159 articles were included and synthesized. Key findings highlight a bidirectional brain-skin axis involving the brain and pituitary, adrenal glands, peripheral nerves and skin. Stress triggers the brain and pituitary to release corticotropin-releasing hormone and adrenocorticotropic hormone; adrenal glands to secrete cortisol, catecholamines and androgens; and peripheral nerves to release neuropeptides such as Substance P and calcitonin gene-related peptide. These are implicated in skin inflammation while skin-derived mediators (cytokines, chemokines, neurotrophins) may disrupt and cross the blood-brain barrier, amplifying neuroinflammation, and psychiatric symptoms. Together, these form a self-sustaining feedback perpetuating both dermatologic and psychological disease.
LIMITATIONS: Much of the mechanistic understanding is derived from animal models; high-quality human data remain limited.
CONCLUSION: Understanding the brain-skin axis identifies therapeutic targets and guides future research on stress-related skin disease.
OBJECTIVE: To synthesize current evidence on brain-skin pathways, emphasizing key mediators and feedback loops that explain how stress exacerbates skin disease and vice versa.
METHODS: A comprehensive search through August 25, 2025, using terms related to brain-skin communication, psychodermatology, and stress-related pathophysiology included both in-vivo and in-vitro animal and human studies.
RESULTS: 159 articles were included and synthesized. Key findings highlight a bidirectional brain-skin axis involving the brain and pituitary, adrenal glands, peripheral nerves and skin. Stress triggers the brain and pituitary to release corticotropin-releasing hormone and adrenocorticotropic hormone; adrenal glands to secrete cortisol, catecholamines and androgens; and peripheral nerves to release neuropeptides such as Substance P and calcitonin gene-related peptide. These are implicated in skin inflammation while skin-derived mediators (cytokines, chemokines, neurotrophins) may disrupt and cross the blood-brain barrier, amplifying neuroinflammation, and psychiatric symptoms. Together, these form a self-sustaining feedback perpetuating both dermatologic and psychological disease.
LIMITATIONS: Much of the mechanistic understanding is derived from animal models; high-quality human data remain limited.
CONCLUSION: Understanding the brain-skin axis identifies therapeutic targets and guides future research on stress-related skin disease.