Intermittent hypoxia (IH) is shared by a wide range of physiological and pathological conditions. However, it is also the hallmark of obstructive sleep apnea (OSA). In the last two decades, OSA has been increasingly identified as a major health risk-factor. This is attributed to its high occurrence and association with a number of co-morbidities, including cardiovascular, cerebrovascular, metabolic, and increased cancer risk, all contributing to increased mortality rates. As such, research has been aimed at identifying the underlying mechanisms for these associations.
Oxidative stress and inflammation are two of the most basic and fundamental mechanisms affected by IH through the involvement of multiple signaling pathways. Yet, based on different severity-dependent changes resulting from frequency, magnitude and chronicity of the IH, the patterns vary considerably, and thereby may initiate diverse and sometimes opposing outcomes. Thus, such diverse IH trajectories can alter a large cluster of physiological measures, signaling pathways and genetic-epigenetic expression. Moreover, the responses to a specific IH paradigm are also cell- and tissue-specific, and the outcomes generally differ from those of sustained hypoxia, even if similar severity and durations are applied.
Although there is an association with various co-morbidities, it is also evident that many OSA patients are free of these co-morbidities. In a number of human, animal and in-vitro studies, some paradigms of IH showed beneficial rather than detrimental effects. This led to the notion that some paradigms of IH may act as a protective mechanism in the form of “ischemic pre-conditioning”. In this well established phenomenon of ischemic pre-conditioning, various paradigms of brief IH applied experimentally, confer protection to tissues and organs rather than inducing damage. The involvement of reactive oxygen species (ROS)-dependent signaling pathways and oxidative stress is implicated both in ischemic pre-conditioning as well as in OSA. Thus, some patterns of IH may confer protection rather than promoting injury.
In this Research Topic, authors are invited to contribute original research articles and reviews to promote ongoing and continued research to further delineate the role of IH in OSA using various experimental models. Authors are also encouraged to submit articles describing diagnostic/predictive biomarkers which can be used as potential targets to develop innovative therapeutic strategies. This can facilitate the identification of patients at a higher risk for co-morbidities and mortality and prioritize the treatment accordingly.
Potential topics for submission, but not limited to:
• Oxidative stress/inflammation, signaling pathways and gene expression at the molecular and cellular levels, in response to various paradigms of IH, in OSA children and adult patients, animal and in-vitro models.
• Cancer and oxidative stress/inflammation, signaling pathways, gene expression and epidemiology in humans and animal models of IH.
• Effects of severity, frequency, and chronicity of IH in OSA patients, animal and in-vitro models - beneficial or detrimental.
• Endothelial dysfunction, atherosclerosis, oxidative stress and ischemic preconditioning in OSA patients, animal and in-vitro models of IH.
• Antioxidants in OSA, animal and in-vitro models of IH.
• Expression of hormones cytokines and biomarkers in various paradigms of IH.
• Determinants of brain susceptibility to IH.
Intermittent hypoxia (IH) is shared by a wide range of physiological and pathological conditions. However, it is also the hallmark of obstructive sleep apnea (OSA). In the last two decades, OSA has been increasingly identified as a major health risk-factor. This is attributed to its high occurrence and association with a number of co-morbidities, including cardiovascular, cerebrovascular, metabolic, and increased cancer risk, all contributing to increased mortality rates. As such, research has been aimed at identifying the underlying mechanisms for these associations.
Oxidative stress and inflammation are two of the most basic and fundamental mechanisms affected by IH through the involvement of multiple signaling pathways. Yet, based on different severity-dependent changes resulting from frequency, magnitude and chronicity of the IH, the patterns vary considerably, and thereby may initiate diverse and sometimes opposing outcomes. Thus, such diverse IH trajectories can alter a large cluster of physiological measures, signaling pathways and genetic-epigenetic expression. Moreover, the responses to a specific IH paradigm are also cell- and tissue-specific, and the outcomes generally differ from those of sustained hypoxia, even if similar severity and durations are applied.
Although there is an association with various co-morbidities, it is also evident that many OSA patients are free of these co-morbidities. In a number of human, animal and in-vitro studies, some paradigms of IH showed beneficial rather than detrimental effects. This led to the notion that some paradigms of IH may act as a protective mechanism in the form of “ischemic pre-conditioning”. In this well established phenomenon of ischemic pre-conditioning, various paradigms of brief IH applied experimentally, confer protection to tissues and organs rather than inducing damage. The involvement of reactive oxygen species (ROS)-dependent signaling pathways and oxidative stress is implicated both in ischemic pre-conditioning as well as in OSA. Thus, some patterns of IH may confer protection rather than promoting injury.
In this Research Topic, authors are invited to contribute original research articles and reviews to promote ongoing and continued research to further delineate the role of IH in OSA using various experimental models. Authors are also encouraged to submit articles describing diagnostic/predictive biomarkers which can be used as potential targets to develop innovative therapeutic strategies. This can facilitate the identification of patients at a higher risk for co-morbidities and mortality and prioritize the treatment accordingly.
Potential topics for submission, but not limited to:
• Oxidative stress/inflammation, signaling pathways and gene expression at the molecular and cellular levels, in response to various paradigms of IH, in OSA children and adult patients, animal and in-vitro models.
• Cancer and oxidative stress/inflammation, signaling pathways, gene expression and epidemiology in humans and animal models of IH.
• Effects of severity, frequency, and chronicity of IH in OSA patients, animal and in-vitro models - beneficial or detrimental.
• Endothelial dysfunction, atherosclerosis, oxidative stress and ischemic preconditioning in OSA patients, animal and in-vitro models of IH.
• Antioxidants in OSA, animal and in-vitro models of IH.
• Expression of hormones cytokines and biomarkers in various paradigms of IH.
• Determinants of brain susceptibility to IH.