Department of Experimental Pathology, University of Bologna, Italy.
Curr Pharm Des. 2010;16(6):609-18. doi: 10.2174/138161210790883840.
A typical feature of ageing is a chronic, low-grade inflammation characterized by a general increase in the production of pro-inflammatory cytokines and inflammatory markers ("inflamm-ageing"). This status may slowly damage one or several organs, especially when unfavorable genetic polymorphisms and epigenetic alterations are concomitant, leading to an increased risk of frailty together with the onset of age-related chronic diseases. The contribution of different tissues (adipose tissue, muscle), organs (brain, liver), immune system and ecosystems (gut microbiota) to age-related inflammation ("inflamm-ageing") will be discussed in this review in the context of its onset/progression leading to site-restricted and systemic effects. Moreover, some of the possible strategies and therapies to counteract the different sources of molecular mediators which lead to the age-related inflammatory phenotype will be presented.
衰老的一个典型特征是慢性、低度炎症,其特征是促炎细胞因子和炎症标志物的普遍增加(“炎症衰老”)。这种状态可能会缓慢损害一个或多个器官,特别是当不利的遗传多态性和表观遗传改变同时存在时,导致虚弱的风险增加以及与年龄相关的慢性疾病的发生。在这篇综述中,将讨论不同组织(脂肪组织、肌肉)、器官(大脑、肝脏)、免疫系统和生态系统(肠道微生物群)对与年龄相关的炎症(“炎症衰老”)的贡献,以及其导致局部和全身影响的发生/进展。此外,还将介绍一些可能的策略和疗法,以对抗导致与年龄相关的炎症表型的不同分子介质的来源。