Computational Models of Reactive Oxygen Species as Metabolic Byproducts and Signal-Transduction Modulators.
Computational Models of Reactive Oxygen Species as Metabolic Byproducts and Signal-Transduction Modulators.
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DOI：
10.3389/fphar.2016.00457
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发表时间：
2016
影响因子：
5.6
通讯作者：
Janes KA
中科院分区：
文献类型：
--
作者：
Pereira EJ;Smolko CM;Janes KA
活性氧（Reactive oxygen species， ROS）广泛参与细胞内信号传导和人类病理，但其确切作用一直难以全面列举和整合。ROS的环境和剂量依赖性细胞内效应可能导致相互矛盾的实验结果和混淆的解释。例如，较低水平的ROS促进细胞信号传导和增殖，而丰富的ROS会对生物分子造成压倒性的损害，导致细胞凋亡或衰老。这些复杂性提出了ROS生物学的许多方面是否可以使用计算建模在一个共同的机制框架下连接的问题。在这里，我们盘点了一些目前的ROS产生或ROS调控信号通路的模型。有几个模型捕捉到了非直觉的观察结果，或者做出了后来被实验证实的预测。仍然需要系统级的分析，将ROS的产生、处理和多个信号转导级联的调制联合起来。
Reactive oxygen species (ROS) are widely involved in intracellular signaling and human pathologies, but their precise roles have been difficult to enumerate and integrate holistically. The context- and dose-dependent intracellular effects of ROS can lead to contradictory experimental results and confounded interpretations. For example, lower levels of ROS promote cell signaling and proliferation, whereas abundant ROS cause overwhelming damage to biomolecules and cellular apoptosis or senescence. These complexities raise the question of whether the many facets of ROS biology can be joined under a common mechanistic framework using computational modeling. Here, we take inventory of some current models for ROS production or ROS regulation of signaling pathways. Several models captured non-intuitive observations or made predictions that were later verified by experiment. There remains a need for systems-level analyses that jointly incorporate ROS production, handling, and modulation of multiple signal-transduction cascades.
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影响因子：
--
作者：
Hamon J;Jennings P;Bois FY
通讯作者：
Bois FY
影响因子：
14.9
作者：
Chorley BN;Campbell MR;Wang X;Karaca M;Sambandan D;Bangura F;Xue P;Pi J;Kleeberger SR;Bell DA
通讯作者：
Bell DA
影响因子：
3.4
作者：
Gauthier, Laura D.;Greenstein, Joseph L.;Winslow, Raimond L.
通讯作者：
Winslow, Raimond L.
影响因子：
4
作者：
Janes, Kevin A.;Lauffenburger, Douglas A.
通讯作者：
Lauffenburger, Douglas A.
影响因子：
3.4
作者：
Bazil, Jason N.;Beard, Daniel A.;Vinnakota, Kalyan C.
通讯作者：
Vinnakota, Kalyan C.