Purpose

Cardiovascular disease (CVD) is the leading cause of death, globally, and its prevalence is only expected to rise due to the increasing incidence of co-morbidities such as obesity and diabetes. Medical treatment of CVD is directed primarily at slowing or reversing the underlying atherosclerotic process by managing circulating lipids with an emphasis on control of low-density lipoprotein (LDL) cholesterol. However, over the past several decades, there has been increasing recognition that chronic inflammation and immune system activation are important contributors to atherosclerosis. This shift in focus has led to the elucidation of the complex interplay between cholesterol and cellular secretion of cytokines involved in CVD pathogenesis. Of the vast array of cytokine promoting atherosclerosis, interferon (IFN)-γ is highly implicated and, therefore, of great interest.

Methods

Literature review was performed to further understand the effect of IFN-γ on the development of atherosclerotic CVD.

Results

IFN-γ, the sole member of the type II IFN family, is produced by T cells and macrophages, and has been found to induce production of other cytokines and to have multiple effects on all stages of atherogenesis. IFN-γ activates a variety of signaling pathways, most commonly the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, to induce oxidative stress, promote foam cell accumulation, stimulate smooth muscle cell proliferation and migration into the arterial intima, enhance platelet-derived growth factor expression, and destabilize plaque. These are just a few of the contributions of IFN-γ to the initiation and progression of atherosclerotic CVD.

Conclusion

Given the pivotal role of IFN-γ in the advancement of CVD, activation of its signaling pathways is being explored as a driver of atherosclerosis. Manipulation of this key cytokine may lead to novel therapeutic avenues for CVD prevention and treatment. A number of therapies are being explored with IFN-γ as the potential target.

中文翻译：

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干扰素-γ 在心血管疾病中的作用：更新。

目的

心血管疾病 (CVD) 是全球范围内的主要死亡原因，并且由于肥胖和糖尿病等合并症的发病率不断增加，预计其患病率只会上升。心血管疾病的药物治疗主要是通过控制循环血脂来减缓或逆转潜在的动脉粥样硬化过程，重点是控制低密度脂蛋白 (LDL) 胆固醇。然而，在过去的几十年里，人们越来越认识到慢性炎症和免疫系统激活是动脉粥样硬化的重要因素。这种关注点的转变导致阐明了胆固醇与参与 CVD 发病机制的细胞因子的细胞分泌之间复杂的相互作用。在促进动脉粥样硬化的大量细胞因子中，干扰素 (IFN)-γ 与此密切相关，因此，

方法

进行文献回顾以进一步了解 IFN-γ 对动脉粥样硬化 CVD 发展的影响。

结果

IFN-γ 是 II 型 IFN 家族的唯一成员，由 T 细胞和巨噬细胞产生，已被发现可诱导其他细胞因子的产生，并对动脉粥样硬化的所有阶段产生多重影响。IFN-γ 激活多种信号通路，最常见的是 Janus 激酶 (JAK)/信号转导和转录激活剂 (STAT) 通路，以诱导氧化应激，促进泡沫细胞积累，刺激平滑肌细胞增殖和迁移到动脉内膜，增强血小板衍生生长因子的表达，并破坏斑块的稳定性。这些只是 IFN-γ 对动脉粥样硬化 CVD 发生和进展的部分贡献。

结论

鉴于 IFN-γ 在 CVD 进展中的关键作用，正在探索激活其信号通路作为动脉粥样硬化的驱动因素。操纵这种关键细胞因子可能会为心血管疾病的预防和治疗开辟新的治疗途径。正在探索以 IFN-γ 作为潜在靶点的多种疗法。