Redox biology in physiology and disease

作者
Matthew Christopher Zimmerman,Adam John Case
出处
期刊:Redox biology [Elsevier BV]
卷期号:27: 101267-101267 被引量:14
标识
DOI:10.1016/j.redox.2019.101267
摘要

Redox biology in physiology and diseaseThe perception of reactive oxygen species (ROS) and free radicals as damaging and toxic byproducts of cellular function has undergone a rapid evolution in the last few decades, which has given rise to the era of redox biology.As new research emerges demonstrating the vital importance of these molecules to normal physiological processes, the concept of ROS acting in a purely detrimental nature is now antiquated.However, this new functional awareness does not mean these reactive species are harmless.To the contrary, dysregulation of the tight control of these volatile messengers may lead to irreversible cellular damage and pathology, which defines true oxidative stress.Yet, the line between physiological redox signaling and oxidative stress remains blurred, and a dearth of literature exists that attempts to firmly delineate these two biological phenomena.In this special issue entitled "Redox Biology in Physiology and Disease," we highlight the work from 11 different research groups investigating the role of redox biology in normal and pathological states.In addition to their contributions to this special issue, these investigators all participated in the inaugural research symposium entitled "Redox Biology in Physiology and Disease" held at the 2018 Experimental Biology Meeting in San Diego, California that was jointly sponsored by the Society for Redox Biology and Medicine (SfRBM) and the American Physiological Society (APS), and is planned to be held at future meetings on a biennial basis.Given that redox biology is pervasive across virtually all cell types and biological systems, the research in this special issue covers many diverse topics such as inflammation, cardiovascular disease, renal function, airway disease, cancer, muscle biology, and neuroscience.For example, Dr. Adam Case and colleagues provided an original research manuscript examining the effects of uncontrolled mitochondrial superoxide (O 2•-) on normal T-lymphocyte physiology [1].Using condi-

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