Could the thromboxane A2 pathway be a therapeutic target for the treatment of obstructive sleep apnea-induced atherosclerosis?

Obstructive sleep apnea (OSA) is characterized by recurrent nocturnal episodes of intermittent hypoxia. This disease is associated with premature atherosclerosis and consequently with increased cardiovascular morbidity and mortality. Atherosclerosis is a chronic inflammatory disease characterized by the activation of some components of the cyclooxygenase pathway. In particular, USA is associated with activation of the thromboxane A(2) (TXA(2))-pathway, in which obesity seems to be a major confounding factor. Moreover, TXA(2)-pathway activation is related to the vascular remodeling associated with USA. In view of the modest effect of the conventional treatment of OSA by continuous positive airway pressure on the cardiovascular risk in obese USA patients, the identification of new therapeutic targets to treat OSA-induced atherosclerosis seems essential. As disruption of the TXA(2)-pathway has been suggested to be of potential interest to prevent atherosclerosis progression, we have reviewed the recent findings on the intricate interaction between the TXA(2)-pathway, chronic intermittent hypoxia and atherosclerosis and suggest promising therapeutic strategies to treat USA-related atherogenesis, including pharmacological and/or nutritional approaches. (c) 2015 Elsevier Inc. All rights reserved.