The plasma membrane of eukaryotic cells defines the boundary to the extracellular environment and, thus provides essential protection from the surroundings. Consequently, disruptions to the cell membrane triggered by excessive mechanical or biochemical stresses pose fatal threats to cells, which they need to cope with to survive. Eukaryotic cells cope with these threats by activating their plasma membrane repair system, which is shared by other cellular functions, and includes mechanisms to remove damaged membrane by internalization (endocytosis), shedding, reorganization of cytoskeleton and membrane fusion events to reseal the membrane. Members of the annexin protein family, which are characterized by their Ca2+-dependent binding to anionic phospholipids, are important regulators of plasma membrane repair. Recent studies based on cellular and biophysical membrane models show that they have more distinct functions in the repair response than previously assumed by regulating membrane curvature and excision of damaged membrane. In cells, plasma membrane injury and flux of Ca2+ ions into the cytoplasm trigger recruitment of annexins including annexin A4 and A6 to the membrane wound edges. Here, they induce curvature and constriction force, which help pull the wound edges together for eventual fusion. Cancer cells are dependent on efficient plasma membrane repair to counteract frequent stress-induced membrane injuries, which opens novel avenues to target cancer cells through their membrane repair system. Here, we discuss mechanisms of single cell wound healing implicating annexin proteins and membrane curvature.

真核细胞的质膜限定了细胞外环境的边界，因此提供了对周围环境的基本保护。因此，由过度的机械或生化压力引起的细胞膜破坏会对细胞造成致命威胁，而细胞必须生存才能应对。真核细胞通过激活其质膜修复系统来应对这些威胁，这是其他细胞功能所共有的，并且包括通过内化作用（内吞作用），细胞骨架的脱落，重组和膜融合事件来重新密封膜以去除受损膜的机制。Annexin蛋白家族的成员，其以Ca2 +依赖性结合阴离子磷脂为特征，是质膜修复的重要调节剂。基于细胞和生物物理膜模型的最新研究表明，它们在修复反应中的功能比以前通过调节膜的曲率和切除受损的膜所假定的功能更为明显。在细胞中，质膜损伤和Ca2 +离子进入细胞质的通量触发包括膜联蛋白A4和A6在内的膜联蛋白募集到膜伤口边缘。在这里，它们会产生曲率和收缩力，有助于将伤口边缘拉在一起，以便最终融合。癌细胞依赖于有效的质膜修复来抵制频繁的应激诱导的膜损伤，这为通过其膜修复系统靶向癌细胞提供了新途径。在这里，我们讨论了涉及膜联蛋白和膜曲率的单细胞伤口愈合机制。质膜损伤和Ca2 +离子进入细胞质的通量触发膜联蛋白（包括膜联蛋白A4和A6）募集到膜伤口边缘。在这里，它们会产生曲率和收缩力，有助于将伤口边缘拉在一起，以便最终融合。癌细胞依赖于有效的质膜修复来抵制频繁的应激诱导的膜损伤，这为通过其膜修复系统靶向癌细胞提供了新途径。在这里，我们讨论了涉及膜联蛋白和膜曲率的单细胞伤口愈合机制。质膜损伤和Ca2 +离子进入细胞质的通量触发膜联蛋白（包括膜联蛋白A4和A6）募集到膜伤口边缘。在这里，它们会产生曲率和收缩力，有助于将伤口边缘拉在一起，以便最终融合。癌细胞依赖于有效的质膜修复来抵制频繁的应激诱导的膜损伤，这为通过其膜修复系统靶向癌细胞提供了新途径。在这里，我们讨论了涉及膜联蛋白和膜曲率的单细胞伤口愈合机制。癌细胞依赖于有效的质膜修复来抵制频繁的应激诱导的膜损伤，这为通过其膜修复系统靶向癌细胞提供了新途径。在这里，我们讨论了涉及膜联蛋白和膜曲率的单细胞伤口愈合机制。癌细胞依赖于有效的质膜修复来抵制频繁的应激诱导的膜损伤，这为通过其膜修复系统靶向癌细胞提供了新途径。在这里，我们讨论了涉及膜联蛋白和膜曲率的单细胞伤口愈合机制。