Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation.
Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation.
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DOI：
10.1016/j.phrs.2020.105212
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发表时间：
2020-11
影响因子：
9.3
通讯作者：
Nagareddy PR
中科院分区：
文献类型：
--
作者：
Sreejit G;Abdel Latif A;Murphy AJ;Nagareddy PR
中性粒细胞计数升高与主要不良心脏事件（包括心肌梗死和心力衰竭早期发展）的风险升高相关。中性粒细胞通过多种机制导致心脏损伤，包括吸引其他免疫细胞和释放炎症介质。最近，一些独立的研究报告了嗜中性粒细胞衍生的alarmin（即S100 A8/A9）在心肌梗死（MI）后诱导炎症和心脏损伤中的因果作用。此外，还观察到MI患者中血清S100 A8/A9水平与主要不良心脏事件（MACE）之间的正相关性，这意味着靶向中性粒细胞或其炎性货物可能有益于减少心力衰竭。然而，与这一观点相反，中性粒细胞和嗜中性粒细胞衍生的S100 A8/A9似乎在炎症的消退中也起着至关重要的作用。因此，更好地了解中性粒细胞如何平衡这些看似相反的功能将使我们能够开发有效的治疗方法，在限制炎症引起的损伤的同时保留炎症消退功能。在这篇综述中，我们特别讨论了嗜中性粒细胞衍生的S100 A8/A9在促进炎症和解决MI的背景下背后的机制。我们还提供了一个关于中性粒细胞如何潜在地靶向改善心脏炎症和随后的损害的观点。
Elevated neutrophil count is associated with higher risk of major adverse cardiac events including myocardial infarction and early development of heart failure. Neutrophils contribute to cardiac damage through a number of mechanisms, including attraction of other immune cells and release of inflammatory mediators. Recently, a number of independent studies have reported a causal role for neutrophil-derived alarmins (i.e. S100A8/A9) in inducing inflammation and cardiac injury following myocardial infarction (MI). Furthermore, a positive correlation between serum S100A8/A9 levels and major adverse cardiac events (MACE) in MI patients was also observed implying that targeting neutrophils or their inflammatory cargo could be beneficial in reducing heart failure. However, contradictory to this idea, neutrophils and neutrophil-derived S100A8/A9 also seem to play a vital role in the resolution of inflammation. Thus, a better understanding of how neutrophils balance these seemingly contrasting functions would allow us to develop effective therapies that preserve the inflammation-resolving function while restricting the damage caused by inflammation. In this review, we specifically discuss the mechanisms behind neutrophil-derived S100A8/A9 in promoting inflammation and resolution in the context of MI. We also provide a perspective on how neutrophils could be potentially targeted to ameliorate cardiac inflammation and the ensuing damage.
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影响因子：
20.1
作者：
Frangogiannis NG
通讯作者：
Frangogiannis NG
影响因子：
37.8
作者：
Croce K;Gao H;Wang Y;Mooroka T;Sakuma M;Shi C;Sukhova GK;Packard RR;Hogg N;Libby P;Simon DI
通讯作者：
Simon DI
影响因子：
2.8
作者：
Chia, Stanley;Nagurney, John T.;Jang, Ik-Kyung
通讯作者：
Jang, Ik-Kyung
影响因子：
24
作者：
Deftereos, Spyridon;Giannopoulos, Georgios;Stefanadis, Christodoulos
通讯作者：
Stefanadis, Christodoulos
影响因子：
15.9
作者：
DONOHUE, DM;REIFF, RH;FINCH, CA
通讯作者：
FINCH, CA