Abstract：
Rapid removal of apoptotic cells by phagocytes, a process known as efferocytosis, is key for the maintenance of tissue homeostasis, the resolution of inflammation, and tissue repair. However, impaired efferocytosis can result in the accumulation of apoptotic cells, subsequently triggering sterile inflammation through the release of endogenous factors such as DNA and nuclear proteins from membrane permeabilized dying cells. Here, we review the molecular basis of the three key phases of efferocytosis, that is, the detection, uptake, and degradation of apoptotic materials by phagocytes. We also discuss how defects in efferocytosis due to the alteration of phagocytes and dying cells can contribute to the low-grade chronic inflammation that occurs during aging, described as inflammaging. Lastly, we explore opportunities in targeting and harnessing the efferocytic machinery to limit aging-associated inflammatory diseases.
摘要：
通过吞噬细胞快速去除凋亡细胞，一个被称为红细胞增多的过程，是维持组织稳态的关键，炎症的解决，和组织修复。然而,受损的细胞凋亡可导致凋亡细胞的积累，随后通过从膜透化的垂死细胞释放内源性因子如DNA和核蛋白引发无菌炎症。这里,我们回顾了efferocytosis的三个关键阶段的分子基础，也就是说,检测，摄取，和吞噬细胞对凋亡物质的降解。我们还讨论了由于吞噬细胞和死亡细胞的改变而导致的红细胞增生缺陷如何导致衰老过程中发生的低度慢性炎症，被描述为发炎。最后,我们探索了靶向和利用白细胞机制来限制衰老相关炎症性疾病的机会.预计药理学和毒理学年度审查的最终在线出版日期，第64卷是2024年1月。请参阅http://www。annualreviews.org/page/journal/pubdates的订正估计数。
