Moreno-Arriola Elizabeth, Cárdenas-Rodríguez Noemí, Coballase-Urrutia Elvia, Pedraza-Chaverri José, Carmona-Aparicio Liliana, Ortega-Cuellar Daniel
Laboratory of Experimental Nutrition, National Institute of Pediatrics, 04530 Mexico City, DF, Mexico.
Laboratory of Neurochemistry, National Institute of Pediatrics, 04530 Mexico City, DF, Mexico.
Oxid Med Cell Longev. 2014;2014:705253. doi: 10.1155/2014/705253. Epub 2014 May 18.
Caenorhabditis elegans is a powerful model organism that is invaluable for experimental research because it can be used to recapitulate most human diseases at either the metabolic or genomic level in vivo. This organism contains many key components related to metabolic and oxidative stress networks that could conceivably allow us to increase and integrate information to understand the causes and mechanisms of complex diseases. Oxidative stress is an etiological factor that influences numerous human diseases, including diabetes. C. elegans displays remarkably similar molecular bases and cellular pathways to those of mammals. Defects in the insulin/insulin-like growth factor-1 signaling pathway or increased ROS levels induce the conserved phase II detoxification response via the SKN-1 pathway to fight against oxidative stress. However, it is noteworthy that, aside from the detrimental effects of ROS, they have been proposed as second messengers that trigger the mitohormetic response to attenuate the adverse effects of oxidative stress. Herein, we briefly describe the importance of C. elegans as an experimental model system for studying metabolic disorders related to oxidative stress and the molecular mechanisms that underlie their pathophysiology.
秀丽隐杆线虫是一种强大的模式生物，对实验研究具有重要价值，因为它可用于在体内代谢或基因组水平上模拟大多数人类疾病。该生物包含许多与代谢和氧化应激网络相关的关键成分，这可能使我们能够增加并整合信息，以了解复杂疾病的病因和机制。氧化应激是影响包括糖尿病在内的多种人类疾病的一个病因。秀丽隐杆线虫与哺乳动物具有非常相似的分子基础和细胞途径。胰岛素/胰岛素样生长因子-1信号通路的缺陷或活性氧水平的升高会通过SKN-1途径诱导保守的二期解毒反应，以对抗氧化应激。然而，值得注意的是，除了活性氧的有害影响外，它们还被认为是触发线粒体应激反应以减轻氧化应激不利影响的第二信使。在此，我们简要描述秀丽隐杆线虫作为研究与氧化应激相关的代谢紊乱及其病理生理学分子机制的实验模型系统的重要性。
