Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.
Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.
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DOI：
10.1016/j.yjmcc.2015.12.018
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发表时间：
2016-02
影响因子：
5
通讯作者：
Ma Y
中科院分区：
文献类型：
--
作者：
Lindsey ML;Iyer RP;Jung M;DeLeon-Pennell KY;Ma Y
尽管目前有最佳的治疗方案，但大约四分之一被诊断为心肌梗死（MI）的患者将继续发展为充血性心力衰竭，心力衰竭的五年死亡率高达50%。因此，阐明心肌梗死后心力衰竭发生的机制是非常必要的。基质金属蛋白酶（MMPs）是心肌梗死后左心室（LV）重构的关键酶。虽然MMPs处理细胞因子和细胞外基质（ECM）底物来调节心肌梗死伤口愈合反应的炎症和纤维化成分，但MMPs也作为上游信号启动物，直接作用于细胞信号级联反应。在这篇综述中，我们总结了目前关于MMP在心肌梗死后左室重构中的作用的文献。我们还确定了当前的知识空白，并提供了实验模板来填补这些空白。更全面地了解MMP的作用，特别是上游信号作用，可能会提供限制不良左室重构的新策略。
Despite current optimal therapeutic regimens, approximately one in four patients diagnosed with myocardial infarction (MI) will go on to develop congestive heart failure, and heart failure has a high five-year mortality rate of 50%. Elucidating mechanisms whereby heart failure develops post-MI, therefore, is highly needed. Matrix metalloproteinases (MMPs) are key enzymes involved in post-MI remodeling of the left ventricle (LV). While MMPs process cytokine and extracellular matrix (ECM) substrates to regulate the inflammatory and fibrotic components of the wound healing response to MI, MMPs also serve as upstream signaling initiators with direct actions on cell signaling cascades. In this review, we summarize the current literature regarding MMP roles in post-MI LV remodeling. We also identify the current knowledge gaps and provide templates for experiments to fill these gaps. A more complete understanding of MMP roles, particularly with regards to upstream signaling roles, may provide new strategies to limit adverse LV remodeling.