Liu L, Stamler J S
Howard Hughes Medical Institute, Duke University Medical Center, Durham NC, 27710, USA.
Cell Death Differ. 1999 Oct;6(10):937-42. doi: 10.1038/sj.cdd.4400578.
Nitric oxide (NO) or related molecules of both endogenous and exogenous origin inhibit programmed cell death in a variety of cells and tissues. This general protective function is largely independent of the apoptotic stimulus. S-nitrosylation of the catalytic-site cysteine of caspases is a well-established and possibly widespread mechanism of enzyme inhibition that protects from cell death. However, NO may inhibit apoptosis by additional mechanisms. The physiological and pathological significance of NO's anti-apoptotic activity remains to be determined in most cases.
一氧化氮(NO)或内源性和外源性相关分子可抑制多种细胞和组织中的程序性细胞死亡。这种普遍的保护功能在很大程度上独立于凋亡刺激。半胱天冬酶催化位点的半胱氨酸发生S-亚硝基化是一种公认的且可能广泛存在的酶抑制机制,可保护细胞免于死亡。然而,NO可能通过其他机制抑制细胞凋亡。在大多数情况下,NO抗凋亡活性的生理和病理意义仍有待确定。