Chronic low-grade elevations of blood-borne cytokines/chemokines in older age tend to associate with frailty in humans. This persistent inflammation is often called “inflammageing” and likely contributes to frailty progression. Preclinical models such as ageing and/or genetically modified mice offer a unique opportunity to mechanistically study how these inflammatory mediators affect frailty. In this review, we summarize and contrast evidence relating cytokines/chemokines to frailty in humans and in mouse models of frailty. In humans and mice, higher levels of the pro-inflammatory cytokine interleukin-6 regularly increased in proportion to the degree of frailty. Evidence linking other cytokines/chemokines to frailty in humans and mice is less certain. The chemokines CXCL-10 and monocyte chemoattractant protein-1 related to frailty across both species, but evidence is limited and inconsistent. Several other cytokines/chemokines, including tumour necrosis factor-α relate to frailty in humans or in mice, but evidence to date is species- and tissue-dependent. It is important for future studies to validate common mechanistic inflammatory biomarkers of frailty between humans and mice. Achieving this goal will accelerate the search for drugs to treat frailty.

老年人血源性细胞因子/趋化因子的慢性低度升高往往与人类的虚弱有关。这种持续的炎症通常被称为“炎症”，可能导致虚弱的进展。衰老和/或转基因小鼠等临床前模型为机械研究这些炎症介质如何影响虚弱提供了独特的机会。在这篇综述中，我们总结并对比了将细胞因子/趋化因子与人类和小鼠衰弱模型中的衰弱相关的证据。在人类和小鼠中，较高水平的促炎细胞因子白细胞介素 6 与虚弱程度成比例地定期增加。将其他细胞因子/趋化因子与人类和小鼠的虚弱联系起来的证据不太确定。趋化因子 CXCL-10 和单核细胞趋化蛋白 1 与这两个物种的虚弱有关，但证据有限且不一致。其他几种细胞因子/趋化因子，包括肿瘤坏死因子-α，与人类或小鼠的虚弱有关，但迄今为止的证据是物种和组织依赖性的。对于未来的研究而言，验证人类和小鼠之间脆弱的常见机制炎症生物标志物非常重要。实现这一目标将加速寻找治疗虚弱的药物。