Department of Cardiology, The Xiamen Cardiovascular Hospital of Xiamen University, Xiamen, Fujian, China.
Department of Cardiac Macrovascular Surgery, The Xiamen Cardiovascular Hospital of Xiamen University, Xiamen, Fujian, China.
Int Immunopharmacol. 2023 Sep;122:110618. doi: 10.1016/j.intimp.2023.110618. Epub 2023 Jul 20.
Aortic dissection, characterized by severe intramural hematoma formation and acute endometrial rupture, is caused by excessive bleeding within the aortic wall or a severe tear within the intimal layer of the aorta, which subsequently promotes the separation or dissection in the layers of the aortic wall. Epidemiological surveys showed that aortic dissection was most observed among those patients from 55 to 80 years of age, with a prevalence of approximately 40 cases per 100,000 individuals per year, posing serious risks to future health and leading to high mortality. Other risk factors of aortic dissection progression contained dyslipidemia, hypertension, and genetic disorders, such as Marfan syndrome. Currently, emerging evidence indicates the pathological progression of aortic dissection is significantly complicated, which is correlated with the aberrant infiltration of pro-inflammatory cells into the aortic wall, subsequently facilitating the apoptosis of vascular smooth muscle cells (VSMCs) and inducing the aberrant expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interferon (IF). Other pro-inflammatory-related cytokines, including the colony-stimulating factor (CSF), chemotactic factor, and growth factor (GF), played an essential function in facilitating aortic dissection. Multiple studies focused on the important relationship between pro-inflammatory cytokines and aortic dissection, which could deepen the understanding of aortic dissection and further guide the therapeutic strategies in clinical practice. The present review elucidated pro-inflammatory cytokines' functions in modulating the risk of aortic dissection are summarized. Moreover, the emerging evidence that aimed to elucidate the potential mechanisms wherebyvarious pro-inflammatory cytokines affected the pathological development of aortic dissection was also listed.
主动脉夹层是一种以严重的壁内血肿形成和急性子宫内膜破裂为特征的疾病，其发生是由于主动脉壁内过度出血或主动脉内膜层的严重撕裂，随后促进了主动脉壁各层的分离或夹层。流行病学调查显示，主动脉夹层最常见于 55 岁至 80 岁的患者，每年每 10 万人中约有 40 例，对未来的健康构成严重威胁，并导致高死亡率。主动脉夹层进展的其他危险因素还包括血脂异常、高血压和遗传疾病，如马凡综合征。目前，新出现的证据表明主动脉夹层的病理进展非常复杂，与炎症细胞异常浸润主动脉壁有关，进而促进血管平滑肌细胞(VSMC)的凋亡，并诱导炎症细胞因子的异常表达，包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和干扰素(IF)。其他与炎症相关的细胞因子，包括集落刺激因子(CSF)、趋化因子和生长因子(GF)，在促进主动脉夹层中发挥了重要作用。多项研究关注了炎症细胞因子与主动脉夹层之间的重要关系，这可以加深对主动脉夹层的理解，并进一步指导临床实践中的治疗策略。本综述总结了促炎细胞因子在调节主动脉夹层风险中的作用。此外，还列出了旨在阐明各种促炎细胞因子如何影响主动脉夹层病理发展的潜在机制的新兴证据。
