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IL-33/ST2 通路作为变应性哮喘中炎症的优势途径,可作为心力衰竭的预测生物标志物。

IL-33/ST2 pathway as upper-hand of inflammation in allergic asthma contributes as predictive biomarker in heart failure.

机构信息

Department of Cardiology, School of Medicine, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.

Department of Cardiology, School of Medicine, Valiasr Hospital, Zanjan University of Medical Sciences, Zanjan, Iran.

出版信息

ESC Heart Fail. 2022 Dec;9(6):3785-3790. doi: 10.1002/ehf2.14111. Epub 2022 Aug 17.

Abstract

Allergic asthma is an inflammatory disorder of the bronchi, and as a major health problem, more than 350 million people suffer from asthma in the world. Many cardiovascular disorders resulted in the impairment of the heart's power to pump blood that leads to the HF. More than 25 million people worldwide live with HF. Accordingly, identifying the biomarkers to predict the onset of future asthma and HF is necessary. IL-33 is an inflammatory cytokine that has the main role in pathophysiology of asthma and HF. Also, in IL-33 receptor, the ST2 is involved in cardiac fibrosis and remodelling in HF and pathogenesis of allergic asthma. Increased sST2 in allergic asthma helps to control inflammation during asthma, but increased sST2 in HF is a predictable biomarker to present risk factor of HF during the time of the patients.

摘要

变应性哮喘是一种支气管炎症性疾病,作为一个主要的健康问题,全球有超过 3.5 亿人患有哮喘。许多心血管疾病导致心脏泵血能力受损,从而导致心力衰竭。全球有超过 2500 万人患有心力衰竭。因此,识别预测未来哮喘和心力衰竭发生的生物标志物是必要的。IL-33 是一种炎症细胞因子,在哮喘和心力衰竭的病理生理学中起主要作用。此外,在 IL-33 受体中,ST2 参与心力衰竭中的心肌纤维化和重塑以及变应性哮喘的发病机制。变应性哮喘中升高的 sST2 有助于控制哮喘期间的炎症,但心力衰竭中升高的 sST2 是预测心力衰竭发生时患者风险因素的一个可预测的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/762f/9773709/41b86d08a4b2/EHF2-9-3785-g001.jpg

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