Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, Italy.
Interdepartmental Centre "L. Galvani" (CIG) and Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Via San Giacomo 12, 40126 Bologna, Italy.
Mech Ageing Dev. 2017 Jul;165(Pt B):129-138. doi: 10.1016/j.mad.2016.12.008. Epub 2016 Dec 27.
Inflammaging is a recent theory of aging originally proposed in 2000 where data and conceptualizations regarding the aging of the immune system (immunosenescence) and the evolution of immune responses from invertebrates to mammals converged. This theory has received an increasing number of citations and experimental confirmations. Here we present an updated version of inflammaging focused on omics data - particularly on glycomics - collected on centenarians, semi-supercentenarians and their offspring. Accordingly, we arrived to the following conclusions: i) inflammaging has a structure where specific combinations of pro- and anti-inflammatory mediators are involved; ii) inflammaging is systemic and more complex than we previously thought, as many organs, tissues and cell types participate in producing pro- and anti-inflammatory stimuli defined "molecular garbage"; iii) inflammaging is dynamic, can be propagated locally to neighboring cells and systemically from organ to organ by circulating products and microvesicles, and amplified by chronic age-related diseases constituting a "local fire", which in turn produces additional inflammatory stimuli and molecular garbage; iv) an integrated Systems Medicine approach is urgently needed to let emerge a robust and highly informative set/combination of omics markers able to better grasp the complex molecular core of inflammaging in elderly and centenarians.
炎症衰老（Inflammaging）是一个最近的衰老理论，最初于 2000 年提出，其中涉及免疫系统衰老（免疫衰老）的数据和概念，以及从无脊椎动物到哺乳动物的免疫反应进化，这些都汇聚到了一起。该理论已经收到了越来越多的引用和实验证实。在这里，我们提出了一个炎症衰老的更新版本，重点是对百岁老人、准百岁老人及其后代的组学数据（特别是糖组学）的研究。因此，我们得出以下结论：i）炎症衰老具有特定的促炎和抗炎介质组合参与的结构；ii）炎症衰老具有系统性，比我们之前认为的更为复杂，因为许多器官、组织和细胞类型参与产生定义为“分子垃圾”的促炎和抗炎刺激物；iii）炎症衰老具有动态性，可以通过循环产物和微泡在局部传播到邻近细胞，并从一个器官系统传播到另一个器官，慢性与年龄相关的疾病会放大这种传播，构成“局部火灾”，进而产生额外的炎症刺激和分子垃圾；iv）迫切需要采用综合系统医学方法，以产生一组稳健且信息量丰富的组学标记物，从而更好地掌握老年和百岁老人炎症衰老的复杂分子核心。
