2021年4月2日，《细胞—代谢》杂志在线发表了美国科学家的一项最新研究成果。来自巴克衰老研究所的Judith Campisi等研究人员合作发现，氧化脂质的生物合成可增强细胞衰老。

研究人员发现，衰老细胞激活了几种氧化脂质的生物合成，这些氧化脂质促进了衰老相关分泌表型（SASP）的形成并增强了增殖停滞。值得注意的是，衰老细胞合成并积累了一种细胞内前列腺素（1a,1b-dihomo-15-deoxy-delta-12,14-prostaglandin J2）。释放这种前列腺素是培养细胞和体内衰老的生物标志物。这种和其他前列腺素D2相关的脂质通过激活RAS信号传导来促进衰老停滞和SASP。这些数据鉴定了一个细胞衰老的重要方面以及检测衰老细胞裂解的方法。 

据了解，细胞衰老是一种应激或损伤反应，会导致永久性增殖抑制和许多生物学活性因子的分泌。这种SASP的特征主要在于参与胚胎发生、伤口愈合、炎症和许多与年龄相关的病理学的分泌蛋白。相比之下，对SASP脂质成分的研究不足。

附：英文原文

Title: Oxylipin biosynthesis reinforces cellular senescence and allows detection of senolysis

Author: Christopher D. Wiley, Rishi Sharma, Sonnet S. Davis, Jose Alberto Lopez-Dominguez, Kylie P. Mitchell, Samantha Wiley, Fatouma Alimirah, Dong Eun Kim, Therese Payne, Andrew Rosko, Eliezer Aimontche, Sharvari M. Deshpande, Francesco Neri, Chisaka Kuehnemann, Marco Demaria, Arvind Ramanathan, Judith Campisi

Issue&Volume: 2021-04-05

Abstract: Cellular senescence is a stress or damage response that causes a permanent proliferativearrest and secretion of numerous factors with potent biological activities. This senescence-associatedsecretory phenotype (SASP) has been characterized largely for secreted proteins thatparticipate in embryogenesis, wound healing, inflammation, and many age-related pathologies.By contrast, lipid components of the SASP are understudied. We show that senescentcells activate the biosynthesis of several oxylipins that promote segments of theSASP and reinforce the proliferative arrest. Notably, senescent cells synthesize andaccumulate an unstudied intracellular prostaglandin, 1a,1b-dihomo-15-deoxy-delta-12,14-prostaglandinJ2. Released 15-deoxy-delta-12,14-prostaglandin J2 is a biomarker of senolysis inculture and in vivo. This and other prostaglandin D2-related lipids promote the senescence arrest andSASP by activating RAS signaling. These data identify an important aspect of cellularsenescence and a method to detect senolysis.

DOI: 10.1016/j.cmet.2021.03.008

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00115-7