HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Douglas, R. M. Articles by Haddad, G. G. Search for Related Content PubMed PubMed Citation Articles by Douglas, R. M. Articles by Haddad, G. G.

REVIEW

Can O₂ Dysregulation Induce Premature Aging?

Robert M. Douglas¹ and Gabriel G. Haddad^1,2,3

¹ Departments of Pediatrics and
² Neuroscience, University of California, San Diego, La Jolla; and
³ Rady Children’s Hospital-San Diego, San Diego, California rdouglas{at}ucsd.edu

Chronic intermittent or episodic hypoxia, as occurs during a number of disease states, can have devastating effects, and prolonged exposure to this hypoxia can result in cell injury or cell death. Indeed, intermittent hypoxia activates a number of signaling pathways that are involved in oxygen sensing, oxidative stress, metabolism, catecholamine biosynthesis, and immune responsiveness. The cumulative effect of these processes over time can undermine cell integrity and lead to a decline in function. Furthermore, the ability to respond adequately to various stressors is hampered, and this is traditionally defined as premature aging or senescence. This review highlights recent advances in our understanding of the cellular and molecular mechanisms that are involved in the response to intermittent hypoxia and the potential interplay among various pathways that may accelerate the aging process.