Immune cell Dilemma in Ischemic Cardiomyopathy: To Heal or Not to Heal.
Immune cell Dilemma in Ischemic Cardiomyopathy: To Heal or Not to Heal.
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DOI：
10.1016/j.cophys.2020.09.002
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发表时间：
2021-03
影响因子：
2.5
通讯作者：
Bansal SS
中科院分区：
文献类型：
--
作者：
Nehra S;Gumina RJ;Bansal SS
炎症是无菌组织损伤的双刃剑，如心肌梗死（MI）。缺血性损伤后，炎症性免疫反应激活修复过程，清除组织碎片，形成稳定的瘢痕，并启动心肌中的血管生成，以实现有效的伤口愈合。然而，不完全的免疫消退或持续的低度炎症导致缺血性心肌病（IC），其特征在于适应不良的组织重塑和左心室扩张。很明显，细胞因子、趋化因子、肾上腺素、消退素以及先天性和适应性免疫系统的微妙平衡对于充分愈合至关重要，因为炎症反应的不充分或过度激活都可能增加破裂发生率或长期加重心功能障碍。在所有参与者中，免疫细胞是最关键的，因为它们不仅是所有炎症蛋白介质的来源，而且也是靶点。然而，与不同免疫亚型相关的表型复杂性、它们的相互依赖性、阶段性激活和不同的功能性通常使得难以将一种免疫细胞的作用与另一种免疫细胞分离。在这篇综述中，我们简要总结了几种先天性和适应性免疫细胞的作用，以使读者熟悉复杂的免疫网络，这些免疫网络决定了MI后伤口愈合的程度和IC期间的适应不良重塑。
Inflammation is a double-edged sword for sterile tissue injury such as in myocardial infarction (MI). After ischemic injury, inflammatory immune responses activate repair processes, clear tissue-debris, form a stable scar and initiate angiogenesis in the myocardium for efficient wound-healing. However, incomplete immune resolution or sustained low-grade inflammation lead to ischemic cardiomyopathy (IC) characterized by maladaptive tissue remodeling and left-ventricular dilatation. It is clear that a delicate balance of cytokines, chemokines, prostaglandins, resolvins, and the innate and adaptive immune systems is critical for adequate healing as both insufficient- or overt-activation of inflammatory responses can either enhance rupture incidence or exacerbate cardiac dysfunction in the long-term. Among all the players, immune cells are the most critical as they are not only a source for all of the inflammatory protein mediators, but are also a target. However, phenotypic complexities associated with different immune subtypes, their interdependence, phasic-activations and varied functionalities often make it difficult to segregate the effects of one immune cell from another. In this review, we briefly summarize the role of several innate and adaptive immune cells to acquaint readers with complex immune-networks that dictate the extent of wound-healing post-MI and maladaptive remodeling during IC.
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影响因子：
20.1
作者：
Ismahil MA;Hamid T;Bansal SS;Patel B;Kingery JR;Prabhu SD
通讯作者：
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影响因子：
8
作者：
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影响因子：
7.3
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影响因子：
2.8
作者：
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通讯作者：
CLEMENT, D
影响因子：
82.9
作者：
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通讯作者：
Penninger, JM