Mini ReviewAging: A revisited theory based on free radicals generated by NOX family NADPH oxidases
Section snippets
Introduction: a short history of reactive oxygen species (ROS) and aging
This hypothesis article is based on two, initially unrelated lines of scientific investigation: (i) designed ROS generation by NOX family NADPH oxidases and (ii) role of ROS in the aging process. Interestingly, the evidence for the existence of designed ROS-generation by NADPH oxidases precedes the concept that ROS are involved in aging. Indeed, the first description of a so-called respiratory burst, i.e. a massive use of oxygen by cells dates back to 1908, when Otto Warburg studied
NOX enzymes
NOX family enzymes are transmembrane electron transporters. They transport electrons from the cytoplasmic electron donor NADPH to molecular oxygen. This process leads to generation of superoxide. Depending on the localization of the respective NOX enzymes (plasma membrane versus intracellular organelles), this superoxide generation occurs either on the outside of the plasma membrane or within the lumen of organelles. However, ROS generated by NOX family NADPH oxidases are able to reach the
Contribution of NOX enzymes to age-related pathologies
As discussed in the chapter above, NOX enzymes have important physiological functions and a complete absence of NOX-dependent ROS generation is therefore detrimental for our organism. The question of this review is however different, namely: do NOX-derived ROS contribute to aging and age-related pathologies? In this chapter, I will summarize our present knowledge on the role of NOX-derived ROS in some relevant age-associated diseases.
Aging and ROS
As discussed in the last chapter, there is little doubt that NOX enzymes are important in the pathogenesis of age-associated diseases. However are they important for the aging process itself? The distinction between age-associated diseases and aging is not always obvious, but it is dear to many researchers in the aging field. It is based on the consideration that even if an old person does not develop Alzheimer’s disease, cardiovascular disease, osteoporosis etc., the person is still old. Thus,
Acknowledgement
This work was supported by a grant from the Swiss National Science Foundation.
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