Zieseniss Anke
Institute of Cardiovascular Physiology, University Medical Center, Georg-August University, Göttingen, Germany.
Hypoxia (Auckl). 2014 Mar 25;2:11-21. doi: 10.2147/HP.S53575. eCollection 2014.
Recent progress in understanding the influence of hypoxia on cell function has revealed new information about the interrelationship between the actin cytoskeleton and hypoxia; nevertheless, details remain cloudy. The dynamic regulation of the actin cytoskeleton during hypoxia is complex, varies in different cells and tissues, and also depends on the mode of hypoxia. Several molecular players and pathways are emerging that contribute to the modulation of the actin cytoskeleton and that affect the large repertoire of actin-binding proteins in hypoxia. This review describes and discusses the accumulated knowledge about actin cytoskeleton dynamics in hypoxia, placing special emphasis on the Rho family of small guanosine triphosphatases (Rho GTPases). Given that RhoA, Rac and Cdc42 are very well characterized, the review is focused on these family members of Rho GTPases. Notably, in several cell types and tissues, hypoxia, presumably via Rho GTPase signaling, induces actin rearrangement and actin stress fiber assembly, which is a prevalent modulation of the actin cytoskeleton in hypoxia.
近年来,在理解缺氧对细胞功能的影响方面取得的进展揭示了有关肌动蛋白细胞骨架与缺氧之间相互关系的新信息;然而,细节仍不清晰。缺氧期间肌动蛋白细胞骨架的动态调节很复杂,在不同细胞和组织中有所不同,并且还取决于缺氧的模式。几种分子参与者和信号通路正在浮现,它们有助于调节肌动蛋白细胞骨架,并影响缺氧状态下大量的肌动蛋白结合蛋白。本综述描述并讨论了关于缺氧时肌动蛋白细胞骨架动力学的累积知识,特别强调小GTP酶(Rho GTP酶)的Rho家族。鉴于RhoA、Rac和Cdc42已得到充分表征,本综述聚焦于Rho GTP酶的这些家族成员。值得注意的是,在几种细胞类型和组织中,缺氧大概通过Rho GTP酶信号传导,诱导肌动蛋白重排和肌动蛋白应力纤维组装,这是缺氧时肌动蛋白细胞骨架的一种普遍调节方式。