Nayak Tapas K, Tilley Douglas G
Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
Curr Opin Physiol. 2021 Feb;19:55-61. doi: 10.1016/j.cophys.2020.09.007. Epub 2020 Sep 15.
Following acute cardiac injury such as myocardial infarction (MI), the controlled activation and recruitment of various leukocytes to the site of tissue damage significantly impacts chronic changes to cardiac structure and function, and ultimately host survival. While recent research has focused primarily on how leukocytes respond to injury, understanding how to effectively modulate their responsiveness to dampen maladaptive inflammation and promote repair processes is not yet fully understood. The complex spatio-temporal migration and activation of leukocytes are largely controlled by various chemokines and their cognate receptors, belonging to the G protein-coupled receptor (GPCR) family. Beyond chemokine receptors, leukocytes express a host of additional GPCRs that have recently been shown to regulate their responsiveness to cardiac injury. In this minireview, we will briefly discuss the impact of chemokine receptors on leukocyte behaviour, with subsequent focus on the most recent advancements in understanding the impact and therapeutic potential of other GPCR classes on leukocyte responses after acute cardiac injury.
在诸如心肌梗死(MI)等急性心脏损伤后,各种白细胞向组织损伤部位的受控激活和募集会显著影响心脏结构和功能的慢性变化,并最终影响宿主的生存。虽然最近的研究主要集中在白细胞如何对损伤做出反应,但如何有效调节它们的反应性以减轻适应性不良炎症并促进修复过程,目前尚未完全了解。白细胞复杂的时空迁移和激活在很大程度上受各种趋化因子及其同源受体控制,这些受体属于G蛋白偶联受体(GPCR)家族。除了趋化因子受体,白细胞还表达许多其他GPCR,最近的研究表明这些受体可调节它们对心脏损伤的反应性。在本综述中,我们将简要讨论趋化因子受体对白细胞行为的影响,随后重点关注在理解其他GPCR类别对急性心脏损伤后白细胞反应的影响和治疗潜力方面的最新进展。