Fulop T, Khalil A, Larbi A
Research center on Aging, University of Sherbrooke, 1036, rue Belvedere sud, Sherbrooke, Qc, J1H 4C4, Canada.
Pathol Biol (Paris). 2012 Feb;60(1):28-33. doi: 10.1016/j.patbio.2011.10.006. Epub 2011 Nov 17.
It is now well accepted that aging is associated with the occurrence of a low-grade inflammation called Inflamm-aging. This leads to the imbalance between the various mediators of the inflammatory response in favour of the pro-inflammatory response represented by pro-inflammatory cytokines and oxidative stress. The question that arises, and is still under investigation, what is the origin of the driving force leading to these changes. One of the current hypotheses is that chronic stimulation of the immune system contributes to the pro-inflammatory shift. The chronic stimulation can be of viral origin such as cytomegalovirus, from tumor antigens or from other sources such as the extracellular matrix, especially from elastin fibres and collagens. Aging and various inflammatory diseases such as atherosclerosis, abdominal aortic aneurysms, chronic obstructive pulmonary diseases (COPD), cancer and type 2 diabetes are characterized by the destruction of elastin fibers and the consequent generation of elastin peptides which are biologically active. This review will describe the putative contribution of elastin peptides to inflamm-aging and extend on their role on immunosenescence, as well as on age-associated chronic inflammatory diseases.
现在人们普遍认为，衰老与一种名为炎症衰老的低度炎症的发生有关。这会导致炎症反应的各种介质之间失衡，有利于以促炎细胞因子和氧化应激为代表的促炎反应。出现的问题，并且仍在研究中，导致这些变化的驱动力的起源是什么。当前的假设之一是免疫系统的慢性刺激促成了促炎转变。这种慢性刺激可能源于病毒，如巨细胞病毒，源于肿瘤抗原或其他来源，如细胞外基质，尤其是弹性纤维和胶原蛋白。衰老以及各种炎症性疾病，如动脉粥样硬化、腹主动脉瘤、慢性阻塞性肺疾病（COPD）、癌症和2型糖尿病，其特征是弹性纤维的破坏以及随之产生的具有生物活性的弹性蛋白肽。本综述将描述弹性蛋白肽对炎症衰老的假定贡献，并扩展其在免疫衰老以及与年龄相关的慢性炎症性疾病中的作用。
