当宿主细胞暴露于外来颗粒时,死细胞,或细胞危害,一个叫做吞噬作用的复杂过程开始了。在这个过程中,巨噬细胞,树突状细胞,嗜中性粒细胞通过扩张它们的膜吞噬目标。凋亡细胞的吞噬作用称为有效细胞作用。这个过程非常重要,因为每天消除数十亿细胞而不会引起炎症。吞噬作用和有效胞吞作用都依赖于Ca2+信号传导。Ca2+渗透通道的一大家族是瞬时受体电位(TRPs),分为9个亚家族。我们旨在回顾它们在吞噬作用中的作用。本综述文章显示,各种TRP通道,如TRPV1、2、3、4、TRPM2、4、7、8、TRPML1、TRPA1、TRPC1、3、5、6在吞噬作用的各个阶段都有作用。它们参与β淀粉样蛋白的吞噬作用,α-突触核蛋白,髓鞘碎片,细菌,和凋亡细胞。特别是,TRPC3和TRPM7有助于细胞凋亡。这些作用是通过改变Ca2+信号传导或靶向胞内酶如Akt来介导的。此外,它们有助于吞噬细胞向目标趋化。尽管有限的研究已经评估了TRP通道在吞噬作用和有效胞吞作用中的作用,他们的研究结果表明,他们在这些过程中发挥着关键作用。在某些情况下,它们的消融完全消除了细胞的吞噬功能。因此,TRP通道是开发调节吞噬作用的新疗法的潜在靶标。
When host cells are exposed to foreign particles, dead cells, or cell hazards, a sophisticated process called phagocytosis begins. During this process, macrophages, dendritic cells, and neutrophils engulf the target by expanding their membranes. Phagocytosis of apoptotic cells is called
efferocytosis. This process is of significant importance as billions of cells are eliminated daily without provoking inflammation. Both phagocytosis and
efferocytosis depend on Ca2+ signaling. A big family of Ca2+ permeable channels is transient receptor potentials (TRPs) divided into nine subfamilies. We aimed to
review their roles in phagocytosis. The present
review article shows that various TRP channels such as TRPV1, 2, 3, 4, TRPM2, 4, 7, 8, TRPML1, TRPA1, TRPC1, 3, 5, 6 have roles at various stages of phagocytosis. They are involved in the phagocytosis of amyloid β, α-synuclein, myelin debris, bacteria, and apoptotic cells. In particular, TRPC3 and TRPM7 contribute to
efferocytosis. These effects are mediated by changing Ca2+ signaling or targeting intracellular enzymes such as Akt. In addition, they contribute to the chemotaxis of phagocytic cells towards targets. Although a limited number of studies have assessed the role of TRP channels in phagocytosis and efferocytosis, their findings indicate that they have critical roles in these processes. In some cases, their ablation completely abolished the phagocytic function of the cells. As a result, TRP channels are potential targets for developing new therapeutics that modulate phagocytosis.