Straub R H, Cutolo M, Zietz B, Schölmerich J
Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University Hospital Regensburg, 93042, Regensburg, Germany.
Mech Ageing Dev. 2001 Sep 30;122(14):1591-611. doi: 10.1016/s0047-6374(01)00289-5.
The immune, endocrine and nervous systems interact with each other by means of cytokines, hormones and neurotransmitters. Interaction is dependent on specific receptors and respective signaling pathways in target cells. During aging, changes occur on many levels of these global systems which depend on oxidative damage, non-enzymatic glycosylation, mitochondrial mutations, defects in cell cycle control, mitotic dysregulation, genome instability, telomere shortening and other chromosomal pathologies. An alteration of the numerical value of a parameter of one system can lead to changes of the numerical value of a variable of another system. In a non-linear dynamic process these changes can contribute to the aging phenotype. Although it is extremely difficult to dissect linear interrelations of three global systems during aging, this review attempts to identify some simple linear pathways. Furthermore, it is demonstrated that chronic inflammatory diseases may accelerate the aging process. This review also reveals that new statistical and computational methods are necessary to unravel the complexity of the aging process.
免疫系统、内分泌系统和神经系统通过细胞因子、激素和神经递质相互作用。这种相互作用依赖于靶细胞中的特定受体和各自的信号通路。在衰老过程中,这些整体系统的多个层面都会发生变化,这些变化取决于氧化损伤、非酶糖基化、线粒体突变、细胞周期控制缺陷、有丝分裂失调、基因组不稳定、端粒缩短和其他染色体病变。一个系统参数数值的改变可能导致另一个系统变量数值的变化。在非线性动态过程中,这些变化可能促成衰老表型。尽管在衰老过程中剖析这三个整体系统的线性相互关系极其困难,但本综述试图找出一些简单的线性途径。此外,研究表明慢性炎症性疾病可能加速衰老过程。本综述还揭示,需要新的统计和计算方法来揭示衰老过程的复杂性。