Thymosin beta 4 regulation of actin in sepsis.
Thymosin beta 4 regulation of actin in sepsis.
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DOI：
10.1080/14712598.2018.1448381
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发表时间：
2018-07
影响因子：
4.6
通讯作者：
Morris DC
中科院分区：
文献类型：
--
作者：
Belsky JB;Rivers EP;Filbin MR;Lee PJ;Morris DC
脓毒症是宿主对感染的失调反应，导致危及生命的器官损伤。胸腺素β 4是一种肌动蛋白结合蛋白，其抑制G-肌动蛋白聚合成F-肌动蛋白，并在静脉内给予脓毒症大鼠时提高死亡率。胸腺素β 4减少炎症介质，降低活性氧，上调抗氧化酶，抗炎基因和抗凋亡酶，使其成为脓毒症研究的有趣蛋白质。作者通过全面的文献检索，总结了肌动蛋白和胸腺素β 4与脓毒症相关的现有知识。败血症导致循环中可测量的F-肌动蛋白水平以及胸腺素β 4浓度降低。据推测，F-放线菌素血症有助于微循环扰动目前在脓毒症患者扰乱层流。鉴于胸腺素β 4抑制F-肌动蛋白的聚合，胸腺素β 4可能通过调节肌动蛋白及其其他抗炎特性降低脓毒症的死亡率，应进一步在脓毒症患者中进行临床试验。
Sepsis is the dysregulated host response to an infection resulting in life-threatening organ damage. Thymosin Beta 4 is an actin binding protein that inhibits the polymerization of G-actin into F-actin and improves mortality when administered intravenously to septic rats. Thymosin Beta 4 decreases inflammatory mediators, lowers reactive oxygen species, up-regulates anti-oxidative enzymes, anti-inflammatory genes, and anti-apoptotic enzymes making it an interesting protein to study in sepsis. The authors summarize the current knowledge of actin and Thymosin Beta 4 as it relates to sepsis via a comprehensive literature search. Sepsis results in measurable levels of F-actin in the circulation as well as a decreased concentration of Thymosin Beta 4. It is speculated that F-actinemia contributes to microcirculatory perturbations present in patients with sepsis by disturbing laminar flow. Given that Thymosin Beta 4 inhibits the polymerization of F-actin, it is possible that Thymosin Beta 4 decreases mortality in sepsis via the regulation of actin as well as its other anti-inflammatory properties and should be further pursued as a clinical trial in humans with sepsis.
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DOI：
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影响因子：
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