Department of Medicine, University of Otago, Dunedin 9016, New Zealand.
Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin 9016, New Zealand.
Int J Mol Sci. 2022 Jul 18;23(14):7916. doi: 10.3390/ijms23147916.
Vascular smooth muscle cells (VSMCs) help to maintain the normal physiological contractility of arterial vessels to control blood pressure; they can also contribute to vascular disease such as atherosclerosis. Ca/calmodulin-dependent kinase II (CaMKII), a multifunctional enzyme with four isoforms and multiple alternative splice variants, contributes to numerous functions within VSMCs. The role of these isoforms has been widely studied across numerous tissue types; however, their functions are still largely unknown within the vasculature. Even more understudied is the role of the different splice variants of each isoform in such signaling pathways. This review evaluates the role of the different CaMKII splice variants in vascular pathological and physiological mechanisms, aiming to show the need for more research to highlight both the deleterious and protective functions of the various splice variants.
血管平滑肌细胞（VSMCs）有助于维持动脉血管的正常生理收缩性以控制血压；它们还可能导致血管疾病，如动脉粥样硬化。钙/钙调蛋白依赖性激酶 II（CaMKII）是一种具有四个同工型和多种选择性剪接变体的多功能酶，有助于 VSMCs 中的许多功能。这些同工型的作用已在许多组织类型中得到广泛研究；然而，它们在脉管系统中的功能在很大程度上仍然未知。研究得更少的是每个同工型的不同剪接变体在这些信号通路中的作用。本综述评估了不同 CaMKII 剪接变体在血管病理和生理机制中的作用，旨在表明需要更多的研究来突出各种剪接变体的有害和保护功能。
