医学
心肌梗塞
心力衰竭
FOXP3型
心脏病学
心室重构
免疫系统
不利影响
内科学
缺血
免疫学
作者
Abdullah Kaplan,Raffaele Altara,Ali H. Eid,George W. Booz,Fouad A. Zouein
标识
DOI:10.1097/fjc.0000000000000436
摘要
Abstract: Myocardial infarction (MI) remains one of the leading causes of heart failure development and death worldwide. To date, interventional and pharmacological therapies are effective in reducing the onset of heart failure and promoting survival. However, progressive maladaptive remodeling post-MI persists in a large fraction of patients resulting in poor prognosis. Immune cell responses and an inflammatory environment largely contribute to adverse cardiac remodeling post-MI. CD4 + FOXP3 + regulatory T cells (Tregs) are known for their immunosuppressive capacity and have been successfully implemented in multiple preclinical studies of permanent and ischemia–reperfusion MI. In this review, we highlight the important cardioprotective role of Tregs at the cardiac tissue, cellular, and molecular level, as well as the most prominent pharmacological venues that could be used to exploit Tregs as a novel therapeutic intervention to lessen myocardial injury post-MI.
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