Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Present address: Department of Internal Medicine, Jacoby Medical Center, New York, New York.
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts; Present address: Department of Psychiatry, Westchester Hospital, Mt Kisco, New York.
Ann Allergy Asthma Immunol. 2014 Apr;112(4):309-16. doi: 10.1016/j.anai.2013.09.017. Epub 2013 Oct 10.
Stress precipitates and worsens not only asthma and atopic dermatitis but also acute coronary syndromes (ACSs), which are associated with coronary inflammation. Evidence linking stress to ACS was reviewed and indicated that activation of coronary mast cells (MCs) by stress, through corticotropin-releasing hormone (CRH) and other neuropeptides, contributes to coronary inflammation and coronary artery disease.
PubMed was searched (2005-2013) for articles using the following keywords: allergies, anaphylaxis, anxiety, coronary arteries, coronary artery disease, C-reactive protein, cytokines, chymase, histamine, hypersensitivity, interleukin-6 (IL-6), inflammation, mast cells, myocardial ischemia, niacin, platelet-activating factor, rupture, spasm, statins, stress, treatment, tryptase, and uroctortin.
Articles were selected based on their relevance to how stress affects ACS and how it activates coronary MCs, leading to coronary hypersensitivity, inflammation, and coronary artery disease.
Stress can precipitate allergies and ACS. Stress stimulates MCs through the activation of high-affinity surface receptors for CRH, leading to a CRH-dependent increase in serum IL-6. Moreover, neurotensin secreted with CRH from peripheral nerves augments the effect of CRH and stimulates cardiac MCs to release IL-6, which is elevated in ACS and is an independent risk factor for myocardial ischemia. MCs also secrete CRH and uroctortin, which induces IL-6 release from cardiomyocytes. The presence of atherosclerosis increases the risk of cardiac MC activation owing to the stimulatory effect of lipoproteins and adipocytokines. Conditions such as Kounis syndrome, mastocytosis, and myalgic encephalopathy/chronic fatigue syndrome are particularly prone to coronary hypersensitivity reactions.
Inhibition of cardiac MCs may be a novel treatment approach.
压力不仅会引发和加重哮喘和特应性皮炎，还会引发与冠状动脉炎症有关的急性冠状动脉综合征（ACS）。有证据表明，压力通过促肾上腺皮质激素释放激素（CRH）和其他神经肽激活冠状动脉肥大细胞（MC），导致冠状动脉炎症和冠状动脉疾病。
在 PubMed 上搜索（2005-2013 年），使用以下关键词的文章：过敏、过敏反应、焦虑、冠状动脉、冠状动脉疾病、C 反应蛋白、细胞因子、糜酶、组织胺、超敏反应、白细胞介素-6（IL-6）、炎症、肥大细胞、心肌缺血、烟酸、血小板激活因子、破裂、痉挛、他汀类药物、应激、治疗、胰蛋白酶和尿皮质素。
根据压力如何影响 ACS 以及如何激活冠状动脉 MC，导致冠状动脉超敏反应、炎症和冠状动脉疾病的相关性，选择文章。
压力可引发过敏和 ACS。压力通过激活肥大细胞表面的高亲和力 CRH 受体来刺激 MC，导致 CRH 依赖性血清 IL-6 增加。此外，与 CRH 一起从周围神经分泌的神经降压素增强了 CRH 的作用，并刺激心脏 MC 释放 IL-6，ACS 中升高，是心肌缺血的独立危险因素。MC 还分泌 CRH 和尿皮质素，诱导心肌细胞释放 IL-6。由于脂蛋白和脂肪细胞因子的刺激作用，动脉粥样硬化的存在增加了心脏 MC 激活的风险。柯尼斯综合征、肥大细胞增多症和肌痛性脑脊髓炎/慢性疲劳综合征等疾病特别容易发生冠状动脉超敏反应。
抑制心脏 MC 可能是一种新的治疗方法。
