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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.
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