Frailty represents a state of vulnerability and increases the risk of negative health outcomes, which is becoming an important public health problem. Over recent years, multiple independent studies have attempted to identify biomarkers that can predict, diagnose, and monitor frailty at the biological level. Among them, several promising candidates have been associated with frailty status including antioxidants and free radicals, and also inflammatory response biomarkers. In this review, we will summarize the more recent advances in this field. Moreover, the identification of scales and measurements to detect and quantify frailty in aged mice, as well as the generation of mouse models, have started to unravel the underlying biological and molecular mechanisms of frailty. We will discuss them here with an emphasis on murine models with overexpression of glucose-6-phosphate dehydrogenase and loss of function of superoxide dismutase and interleukin 10, which reveal that altered oxidative stress and inflammation pathways are involved in the physiopathology of frailty. In summary, we provide the current available evidence, from both human cohorts and experimental animal models, that highlights oxidative damage and inflammation as relevant biomarkers and drivers of frailty.

中文翻译：

---

根据人体研究和小鼠模型，氧化应激和脆弱性炎症的相关性。

脆弱代表脆弱状态，并增加了负面健康后果的风险，这正成为重要的公共卫生问题。近年来，多项独立研究试图鉴定可在生物学水平上预测，诊断和监测衰弱的生物标志物。其中，一些有前途的候选物与体弱状态有关，包括抗氧化剂和自由基，以及炎症反应生物标志物。在本文中，我们将总结该领域的最新进展。此外，用于检测和量化衰老小鼠的脆弱性的量表和测量方法以及小鼠模型的产生，已经开始揭示脆弱性的潜在生物学和分子机制。我们将在这里重点讨论鼠模型中的葡萄糖-6-磷酸脱氢酶的过表达以及超氧化物歧化酶和白介素10的功能丧失，这些模型揭示了氧化应激和炎症途径的改变与体弱的生理病理有关。总之，我们提供了来自人类队列和实验动物模型的当前可用证据，这些证据突出了氧化损伤和炎症作为相关的生物标志物和脆弱的驱动力。