A Review of Biological Pathways of Chronic Stress as a Risk Hub for Multiple Psychosomatic Diseases From the Perspective of Clinical Nursing
Abstract
Chronic stress has emerged as a critical global public health threat, acting as a risk hub that mediates the onset and progression of diverse psychosomatic diseases (e.g., cardiovascular diseases, mental disorders, metabolic syndrome, and even cancer) through interconnected biological pathways. This review systematically elaborates on the core biological mechanisms underlying chronic stress-induced psychosomatic dysfunction, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation, autonomic nervous system (ANS) imbalance, abnormal inflammatory responses, and excessive oxidative stress-with precise corrections to factual descriptions of neuroendocrine signaling. From a clinical nursing perspective, we critically evaluate existing evidence for each pathway, identify key gaps in current research, and strengthen the mechanistic link between targeted nursing interventions and biological pathway modulation. We also integrate recent advances in neuro-immuno-endocrinology (e.g., peripheral stress response in the skin) and photo-neuro-immuno-endocrinology, and supplement evidence for stress-cancer crosstalk. Additionally, we clarify the definition of the "risk hub" concept, add a brief literature selection methodology, and propose visualized pathway schematics to enhance clarity. This review provides a refined theoretical foundation for clinical nurses to conduct precise risk stratification, develop pathway-specific intervention plans, and implement personalized care, ultimately advancing early prevention and prognosis improvement of chronic stress-related psychosomatic diseases.
Fields of Study & Subjects
Stress Responses and Cortisol
Cancer
Stress
Anesthesia
and Immune Response
Tryptophan and brain disorders
Publication details
- Journal / source
- Nursing Research and Practice
- Publisher
- Wiley
- Volume
- 2026
- Issue
- 1
- Pages
- 9570388–9570388
- Publication date
- 1 January 2026
- Language
- EN