van Echten-Deckert Gerhild, Hagen-Euteneuer Nadine, Karaca Ilker, Walter Jochen
Life and Medical Sciences (LIMES), Membrane Biology and Lipid Biochemistry Unit at the Kekulé-Institute, University of Bonn, Bonn, Germany.
Cell Physiol Biochem. 2014;34(1):148-57. doi: 10.1159/000362991. Epub 2014 Jun 16.
Sphingosine-1-phosphate (S1P), an evolutionary conserved bioactive lipid, is essential for brain development, but might also exert detrimental effects in terminally differentiated post-mitotic neurons. Its concentration in the brain is tightly regulated by specific kinases and phosphatases, and mainly by the S1P degrading enzyme, S1P-lyase (S1PL). The role of S1P in neurons was initially studied in primary cultures by using structural analogues. During the last 3 years generation of a S1PL deficient mouse model substantially promoted our knowledge on the functional role of S1P metabolism in the brain, and its potential relation to neurodegenerative diseases. However, our understanding of the molecular mechanisms that underlie the physiological and pathophysiological actions of S1P in neurons remains rather scarce.
鞘氨醇-1-磷酸（S1P）是一种进化上保守的生物活性脂质，对大脑发育至关重要，但在终末分化的有丝分裂后神经元中也可能产生有害影响。其在大脑中的浓度受到特定激酶和磷酸酶的严格调控，主要由S1P降解酶S1P裂解酶（S1PL）调控。S1P在神经元中的作用最初是通过使用结构类似物在原代培养物中进行研究的。在过去3年中，S1PL缺陷小鼠模型的产生极大地促进了我们对S1P代谢在大脑中的功能作用及其与神经退行性疾病潜在关系的认识。然而，我们对S1P在神经元中的生理和病理生理作用所基于的分子机制的理解仍然相当匮乏。
