释 义 adj. [生物] 血管的
短 语 vascular tissue 维管组织；血管组织；脉管组织 vascular resistance 血管阻力
同根词 adj. vasodilator [生理][药] 血管扩张的 vasoconstrictor 血管收缩的
n. vasoconstriction [生理] 血管收缩
例 句 To study the value of the vascular interventional embolization therapy for the urinary tract hemorrhage.
释 义 adj. 内皮的
同根词 n. endothelium [解剖] 内皮；内覆组织
例 句 In hemangiomas the endothelial cells multiply at an abnormally rapid rate.
释 义 n. 细胞；电池；蜂房的巢室；单人小室
短 语 cell cycle 细胞周期 cell proliferation 细胞增殖，细胞增生
同根词 n. cellularity 细胞性；多孔性；细胞结构
例 句 Inside every cell in all organisms, there are strands of DNA.
作者： Aleksandra Kopacz
Premature senescence, a death escaping pathway for cells experiencing stress, is conducive to aging and cardiovascular diseases. The molecular switch between senescent and apoptotic fate remains, however, poorly recognized. Nrf2 is an important transcription factor orchestrating adaptive response to cellular stress. Here, we show that both human primary endothelial cells (ECs) and murine aortas lacking Nrf2 signaling are senescent but unexpectedly do not encounter damaging oxidative stress. Instead, they exhibit markedly increased S-nitrosation of proteins. A functional role of S-nitrosation is protection of ECs from death by inhibition of NOX4-mediated oxidative damage and redirection of ECs to premature senescence. S-nitrosation and senescence are mediated by Keap1, a direct binding partner of Nrf2, which colocalizes and precipitates with nitric oxide synthase (NOS) and transnitrosating protein GAPDH in ECs devoid of Nrf2. We conclude that the overabundance of this “unrestrained” Keap1 determines the fate of ECs by regulation of S-nitrosation and propose that Keap1/GAPDH/NOS complex may serve as an enzymatic machinery for S-nitrosation in mammalian cells.