Redox Signaling in Aging and Age-Related Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 2392

Special Issue Editors


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Guest Editor
State Key Laboratory for Structural Chemistry of Unstable and Stable Species, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190, China
Interests: free radicals; nanomaterials; reactive oxygen species; antioxidants; aging; age-related diseases

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Guest Editor
1. School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266071, China
2. School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China
Interests: aging; age-related diseases; antioxidants; mitochondrial metabolism
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Guest Editor
Key Laboratory of Bio-Resources and Eco-Environment of Ministry of Education, College of Life Science, Sichuan University, Chengdu 610064, China
Interests: aging; life span; lipid metabolism; ferroptosis; antioxidants; age-related diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging not only leads to an increased probability of death but also results in a decline in the quality of life due to frailty, disability and age-related diseases (ARDs) in humans. In fact, aging is the major risk factor for a number of chronic ARDs which have significant economic, health and social impacts. Therefore, strategies to slow or delay the aging process and which benefit both the health span and ARDs are critically needed.

To develop such strategies requires a better understanding of the biochemical changes that constitute the basic biology of aging before we can establish any effective interventions. Despite the long-standing controversy over the free radical theory of aging, it is well accepted that redox signals, which include signals of reactive oxygen species (ROS), reactive nitrogen species (RNS), reactive sulfur species (RSS) and more, play essential roles in regulating the aging process and, therefore, have significant clinical implications for ARDs. Greater knowledge of redox signaling in aging will provide us with more tools to slow aging processes which have proven to be intractable.

We are excited to organize this Special Issue which focuses on the regulation of aging and ARDs by redox signals. We hope that the basic science and clinical studies presented in this Special Issue will advance our knowledge and foster new ways to reduce the burden of ARDs and extend the health span.

Prof. Dr. Yang Liu
Prof. Dr. Jiankang Liu
Prof. Dr. Ke Liu
Guest Editors

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Keywords

  • redox
  • aging
  • age-related diseases
  • life span
  • health span
  • free radicals
  • reactive oxygen species
  • nitrogen oxide
  • hydrogen sulfide
  • cell death

Published Papers (1 paper)

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Research

10 pages, 2052 KiB  
Article
Caffeine Decreases Hepcidin Expression to Alleviate Aberrant Iron Metabolism under Inflammation by Regulating the IL-6/STAT3 Pathway
by Zhong-Da Li, Meng-Yu Geng, Song-Rui Dou, Xuan Wang, Zi-Han Zhang and Yan-Zhong Chang
Life 2022, 12(7), 1025; https://doi.org/10.3390/life12071025 - 10 Jul 2022
Cited by 3 | Viewed by 1692
Abstract
Caffeine is well-known as a psychostimulant, and it can also be beneficial in numerous diseases such as diabetes and different types of cancer. Previous studies have shown that caffeine can have a protective role in bacterial infection-induced inflammation and hyperoxia-mediated pulmonary inflammation. Hepcidin, [...] Read more.
Caffeine is well-known as a psychostimulant, and it can also be beneficial in numerous diseases such as diabetes and different types of cancer. Previous studies have shown that caffeine can have a protective role in bacterial infection-induced inflammation and hyperoxia-mediated pulmonary inflammation. Hepcidin, which is regulated by the IL-6/STAT3 inflammation pathway, is a peptide hormone that maintains systemic iron homeostasis. We hypothesized that caffeine’s effects on inflammation may also influence hepcidin production and therefore systemic iron metabolism. To this end, we treated 2-month-old mice with caffeine by daily intragastric administration for 7 days, administering intraperitoneal LPS after the final caffeine treatment. Twelve hours after LPS treatment the mice were euthanized, and tissues were collected. We found that caffeine decreased hepatic hepcidin expression and attenuated LPS-induced hepatic hepcidin overexpression. IL-6 expression and STAT3 phosphorylation were also reduced upon caffeine administration. Additionally, hepatic and splenic FPN1 levels increased after caffeine treatment, leading to lower iron levels in liver and spleen tissues and higher iron levels in serum. Caffeine also prevented the increase in spleen weight and decrease in body weight after LPS treatment. Together, our findings suggest that caffeine decreases hepcidin expression via inhibiting inflammation and the activation of the IL-6/STAT3 pathway, thus presenting an attractive, potential therapeutic for the treatment of anemia of inflammation. Full article
(This article belongs to the Special Issue Redox Signaling in Aging and Age-Related Diseases)
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