Allergic asthma aggravates angiotensin Ⅱ-induced cardiac remodeling in mice.
Allergic asthma aggravates angiotensin Ⅱ-induced cardiac remodeling in mice.
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DOI：
10.1016/j.trsl.2022.01.005
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发表时间：
2022-01
期刊：
影响因子：
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通讯作者：
Chi Geng;Yufan Feng;Yang Yang-Yang;Hongqin Yang;Zhiwei Li;Yaqin Tang;Jing Wang;Hongmei Zhao
中科院分区：
文献类型：
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作者：
Chi Geng;Yufan Feng;Yang Yang-Yang;Hongqin Yang;Zhiwei Li;Yaqin Tang;Jing Wang;Hongmei Zhao
心血管疾病仍然是全球主要的死亡原因，心力衰竭(HF)是其晚期。哮喘是最常见的慢性病之一，据报道，它与心血管疾病的风险增加有关。然而，哮喘和心力衰竭之间的联系很少被研究，哮喘影响心力衰竭的可能机制也不清楚。本研究旨在探讨哮喘对心力衰竭的影响及其可能机制。我们分析了国家健康和营养检查调查的数据，发现哮喘患者中心力衰竭的患病率更高，并确定心力衰竭与哮喘之间存在独立的联系。随后，我们建立了卵白蛋白致敏的过敏性哮喘小鼠模型和血管紧张素Ⅱ输注诱导的心脏重构模型，以探讨哮喘对在体心脏重构的影响。结果表明，OVA诱发的哮喘损害了小鼠的心功能，加重了心脏重构。我们还发现卵白蛋白致敏增加了血清免疫球蛋白E和心脏免疫球蛋白E受体(FcεR1)的表达水平，并增强了心脏Ig E-FcεR1下游信号分子的激活。重要的是，使用FcεR1缺陷小鼠或抗ε抗体阻断Ig E-Fc Fc Ig R1可防止哮喘引起的心功能下降，并减轻心脏重塑。这些发现证明了过敏性哮喘对心脏的不良影响，并提示抗IgE治疗在哮喘合并心脏疾病治疗中的潜在应用。
Cardiovascular disease remains the leading cause of death globally, and heart failure (HF) represents its terminal stage. Asthma, one of the most common chronic diseases, has been reported to be associated with an increased risk of cardiovascular disease. However, the link between asthma and HF has rarely been studied, and the possible mechanisms by which asthma affects HF are unclear. This study aimed to explore the influence of asthma on HF and the possible mechanisms. We analyzed data from the National Health and Nutrition Examination Survey and found a higher prevalence of HF among asthmatic individuals, and identified an independent association between HF and asthma. Subsequently, we produced mice with concurrent ovalbumin (OVA) sensitization-induced allergic asthma and angiotensin Ⅱ infusion-induced cardiac remodeling to explore the effect of asthma on cardiac remodelingin vivo. The results showed that OVA-induced asthma impaired heart function and aggravated cardiac remodeling in mice. We also found that OVA sensitization increased the expression levels of immunoglobulin E (IgE) in serum and IgE receptor (FcεR1) in the heart, and enhanced the activation of downstream signaling molecules of IgE-FcεR1 in the heart. Importantly, blockage of IgE-FcεR1 using FcεR1-deficient mice or an anti-IgE antibody prevented asthma-induced decline of cardiac function, and alleviated cardiac remodeling. These findings demonstrate the adverse effects of allergic asthma on the heart, and suggest the potential application of anti-IgE therapy in the treatment of asthma complicated with heart conditions.