Review Volume 12, Issue 10 pp 9982—9999
Relevance of oxidative stress and inflammation in frailty based on human studies and mouse models
- 1 Group of Cellular Oncology, Biodonostia Health Research Institute, San Sebastian, Spain
- 2 CIBER of Frailty and Healthy Aging (CIBERfes), Spain
- 3 Group of Multiple Sclerosis, Biodonostia Health Research Institute, San Sebastian, Spain
- 4 Group of Primary Health, Biodonostia Health Research Institute, San Sebastian, Spain, Health Services Research on Chronic Patients Network (REDISSEC), Spain
- 5 Spanish Network of Multiple Sclerosis, Spain
- 6 IKERBASQUE, Basque Foundation, Bilbao, Spain
Received: January 29, 2020 Accepted: April 28, 2020 Published: May 27, 2020https://doi.org/10.18632/aging.103295
How to Cite
Copyright © 2020 Álvarez-Satta et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.