Valcovici Mihaela, Iacob Mihai Sorin, Sharma Abhinav, Pah Ana Maria, Marin-Bancila Lucretia, Berceanu Marcel Mihai Vaduva, Velimirovici Milan Daniel, Dinu Anca-Raluca, Drăgan Simona Ruxanda, Kundnani Nilima Rajpal
Department VI-Cardiology, "Victor Babeş" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
Doctoral School, "Victor Babeş" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
Life (Basel). 2025 Jun 16;15(6):964. doi: 10.3390/life15060964.
: Cardiovascular disorders, especially atherosclerosis, have been associated with allergic inflammation. In addition to traditional inflammatory responses, there is evidence that the development and instability of coronary artery plaque may be influenced by effector cells of allergic inflammation. This review examines the phases of allergic pathology, the immunological mechanisms of atherosclerosis, and the clinical link between allergic diseases (asthma, atopic dermatitis, allergic rhinitis, and food allergy) and cardiovascular disease (CVD), along with future therapeutic perspectives. : A literature search was conducted in PubMed, Google scholar; ScienceDirect, Scopus, and studies published between 2014-2024 were taken into consideration. Keywords included allergic inflammation, eosinophils, mast cells, reactive oxygen species, atherosclerosis, Th2 cells, and cytokines. Epidemiological studies and review articles were included. : Emerging evidence suggests that allergic inflammation contributes to atherosclerosis through interconnected mechanisms such as eosinophil activation, reactive oxygen species production, mast cell degranulation, and endothelial dysfunction. Th2-driven immune responses, which are mediated by cytokines such as IL-4, IL-5, and IL-13, as well as eosinophil activity and mast cell degranulation, play a crucial role in vascular inflammation and plaque progression. Additionally, changes in lipid metabolism contribute to this process. Epidemiological studies support this connection, indicating that patients with chronic allergic conditions such as asthma, allergic rhinitis, food allergy, and atopic dermatitis experience increased cardiovascular morbidity. However, most current data are observational, and our understanding of the underlying mechanisms in humans remains limited, often relying on insights gained from preclinical models. : A potential mechanism for cardiovascular risk is suggested by the interaction between atherosclerosis and allergic inflammation. Promising alternatives for treating allergic inflammation and cardiovascular issues include novel treatments like cytokine inhibitors, mast cell stabilizers, and biologics that target certain pathways. Further research is necessary to see whether concentrating on allergy pathways could lead to innovative treatments for cardiovascular disorders or vice versa.
心血管疾病,尤其是动脉粥样硬化,与过敏性炎症有关。除了传统的炎症反应外,有证据表明冠状动脉斑块的形成和不稳定性可能受到过敏性炎症效应细胞的影响。本综述探讨了过敏性病理的阶段、动脉粥样硬化的免疫机制、过敏性疾病(哮喘、特应性皮炎、过敏性鼻炎和食物过敏)与心血管疾病(CVD)之间的临床联系以及未来的治疗前景。:在PubMed、谷歌学术、ScienceDirect、Scopus中进行了文献检索,并考虑了2014年至2024年间发表的研究。关键词包括过敏性炎症、嗜酸性粒细胞、肥大细胞、活性氧、动脉粥样硬化、Th2细胞和细胞因子。纳入了流行病学研究和综述文章。:新出现的证据表明,过敏性炎症通过嗜酸性粒细胞活化、活性氧产生、肥大细胞脱颗粒和内皮功能障碍等相互关联的机制促成动脉粥样硬化。由IL-4、IL-5和IL-13等细胞因子介导的Th2驱动的免疫反应,以及嗜酸性粒细胞活性和肥大细胞脱颗粒,在血管炎症和斑块进展中起关键作用。此外,脂质代谢的变化也促成了这一过程。流行病学研究支持这种联系,表明患有慢性过敏性疾病如哮喘、过敏性鼻炎、食物过敏和特应性皮炎的患者心血管发病率增加。然而,目前的大多数数据都是观察性的,我们对人类潜在机制的理解仍然有限,常常依赖于从临床前模型中获得的见解。:动脉粥样硬化与过敏性炎症之间的相互作用提示了一种心血管风险的潜在机制。治疗过敏性炎症和心血管问题的有前景的替代方法包括细胞因子抑制剂、肥大细胞稳定剂和靶向某些途径的生物制剂等新型治疗方法。有必要进一步研究专注于过敏途径是否能带来心血管疾病的创新治疗方法,反之亦然。