Inducible nitric oxide synthase in human diseases
Inducible nitric oxide synthase in human diseases
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DOI：
10.1046/j.1365-2249.1998.00648.x
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发表时间：
1998-08
影响因子：
4.6
通讯作者：
K. Kröncke;K. Fehsel;V. Kolb‐Bachofen
中科院分区：
文献类型：
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作者：
K. Kröncke;K. Fehsel;V. Kolb‐Bachofen
自20世纪80年代末发现一氧化氮（NO）作为一种生物活性分子以来，已发现其在生物体的许多部分中作为信号分子以及先天性免疫应答的细胞毒性或调节效应分子发挥重要作用。信号分子NO在组成型表达的内皮NO合酶（eNOS）或神经元NO合酶（nNOS）的酶激活后短时间（数秒至数分钟）按需合成。相比之下，诱导型NO合酶（iNOS）仅在细胞活化后表达，然后在相对长的时间段（数小时至数天）内产生NO。因此，受调节的短脉冲合成与恒定的NO产生区分了NO的生理和病理生理作用（综述见[1]）。由于人单核细胞在体外激活时不产生大量的NO，因此iNOS在人类疾病中的表达长期以来一直受到质疑。然而，在过去的3年中，数据已经积累了各种人类疾病或病症中的iNOS表达。我们在这里试图回顾我们目前的理解，在人类疾病中的作用iNOS。
Since its discovery as a biologically active molecule in the late 1980s, nitric oxide (NO) has been found to play an important role as signal molecule in many parts of the organism as well as cytotoxic or regulatory effector molecule of the innate immune response. The signal molecule NO is synthesized on demand for short periods of time (seconds to minutes) following enzyme activation of constitutively expressed endothelial NO synthase (eNOS) or neuronal NO synthase (nNOS). In contrast, the inducible NO synthase (iNOS) is expressed after cell activation only and then produces NO for comparatively long periods of time (hours to days). Thus, regulated short pulsative synthesis versus constant NO production differentiates between physiological and pathophysiological actions of NO (for review see [1]). As human monocytes in contrast to rodent ones do not produce large amounts of NO when activated in vitro, iNOS expression in human diseases has long been questionable. However, in the last 3 years data have accumulated on iNOS expression in a variety of human diseases or disorders. We here try to review our current understanding of the role of iNOS in human diseases.