International Journal of Molecular Sciences· 2025Q1· Derleme
Kronik Stres ve Otoimmünite: HPA Ekseni ve Kortizol Disregülasyonunun Rolü
Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation
- 112atıf
- Q1SCImago
- 2025yıl
Kısa özet
Kronik stres, HPA eksenini ve kortizol sinyal iletimini bozarak bağışıklık toleransını bozar ve otoimmüniteyi destekleyen pro-inflamatuar bir durumu teşvik eder.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Ana noktalar
- Kronik stres, HPA ekseni geri bildirimini bozar ve glukokortikoid reseptör direncine neden olur.
- Kronik stres altında kortizol disregülasyonu, pro-inflamatuar bir durumu ve sitokin dengesizliğini teşvik eder.
- Bu bağışıklık dengesizliği koruyucu mekanizmaları zayıflatır ve otoimmünite gelişimini destekler.
- HPA ekseni disfonksiyonu, lupus, romatoid artrit ve multipl skleroz gibi otoimmün hastalıklarla ilişkilidir.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Özet (abstract)
Autoimmune diseases are chronic inflammatory conditions characterized by the breakdown of immune tolerance to self-antigens. While genetic and environmental factors play key roles, growing evidence highlights chronic stress as a significant contributor to immune dysregulation through its impact on the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis, primarily via cortisol secretion, serves as the major neuroendocrine mediator of stress responses, influencing both immune regulation and systemic homeostasis. This review synthesizes current literature on HPA axis physiology, the mechanisms of cortisol signaling, and the maladaptive effects of chronic stress. Emphasis is placed on clinical and experimental findings linking HPA dysfunction to immune imbalance and autoimmunity, as well as organ-specific consequences across neuroimmune, endocrine, cardiovascular, gastrointestinal, integumentary, and musculoskeletal systems. Chronic stress leads to impaired HPA axis feedback, glucocorticoid receptor resistance, and paradoxical cortisol dysregulation, fostering a pro-inflammatory state. This dysregulation promotes cytokine imbalance, weakens protective immune mechanisms, and shifts the immune response toward autoimmunity. Evidence from both human and animal studies associates persistent HPA dysfunction with diseases such as systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. HPA axis dysregulation under chronic stress constitutes a critical mechanistic link between psychological stress and autoimmune disease. Understanding these pathways provides opportunities for therapeutic interventions, including stress management, lifestyle modification, and neuroendocrine-targeted treatments. Future research should focus on multi-omics and longitudinal approaches to clarify the reversibility of HPA alterations and identify resilience factors.
Yazarların özeti; kaynağından alınmıştır. International Journal of Molecular Sciences, 2025 · DOI ↗
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Alan: Davranışsal Sinirbilim
Behavioral NeuroscienceNeuroscience