Jakab Martin, Fürst Johannes, Gschwentner Martin, Bottà Guido, Garavaglia Maria-Lisa, Bazzini Claudia, Rodighiero Simona, Meyer Giuliano, Eichmueller Sonja, Wöll Eichmüller, Chwatal Sabine, Ritter Markus, Paulmichl Markus
Institute of Physiology, University of Innsbruck, Austria.
Cell Physiol Biochem. 2002;12(5-6):235-58. doi: 10.1159/000067895.
Cell volume alterations are involved in numerous cellular events like epithelial transport, metabolic processes, hormone secretion, cell migration, proliferation and apoptosis. Above all it is a need for every cell to counteract osmotic cell swelling in order to avoid cell damage. The defence against excess cell swelling is accomplished by a reduction of the intracellular osmolarity by release of organic- or inorganic osmolytes from the cell or by synthesis of osmotically less active macromolecules from their specific subunits. De-spite the large amount of experimental data that has accumulated, the intracellular mechanisms underlying the sensing of cell volume perturbations and the activation of volume compensatory processes, commonly summarized as regulatory volume decrease (RVD), are still only partly revealed. Moving into this field opens a complex scenario of molecular rearrangements and interactions involving intracellular messengers such as calcium, phosphoinositides and inositolphosphates as well as phosphoryla-tion/dephosphorylation processes and cytoskeletal reorganization with marked cell type- and tissue specific variations. Even in one and the same cell type significant differences regarding the activated pathways during RVD may be evident. This makes it virtually im-possible to unambigously define common sensing- and sinaling pathways used by differ-ent cells to readjust their celll volume, even if all these pathways converge to the activa-tion of comparatively few sets of effectors serving for osmolyte extrusion, including ion channels and transporters. This review is aimed at providing an insight into the manifold cellular mechanisms and alterations occuring during cell swelling and RVD.
细胞体积的改变涉及众多细胞活动，如上皮运输、代谢过程、激素分泌、细胞迁移、增殖和凋亡。最重要的是，每个细胞都需要抵抗渗透性细胞肿胀以避免细胞损伤。通过从细胞中释放有机或无机渗透溶质，或通过从其特定亚基合成渗透活性较低的大分子来降低细胞内渗透压，从而实现对过度细胞肿胀的防御。尽管已经积累了大量的实验数据，但细胞体积扰动感知和体积补偿过程激活（通常概括为调节性体积减小，RVD）的细胞内机制仍仅部分被揭示。进入这个领域会开启一个复杂的分子重排和相互作用的场景，涉及细胞内信使如钙、磷酸肌醇和肌醇磷酸，以及磷酸化/去磷酸化过程和细胞骨架重组，且具有明显的细胞类型和组织特异性差异。即使在同一种细胞类型中，RVD过程中激活的途径也可能存在显著差异。这使得几乎不可能明确界定不同细胞用于重新调节其细胞体积的共同传感和信号传导途径，即使所有这些途径都汇聚到相对较少的几组效应器的激活上，这些效应器用于渗透溶质的排出，包括离子通道和转运体。这篇综述旨在深入了解细胞肿胀和RVD过程中发生的多种细胞机制和变化。
