Minerva medica
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Sleep disordered breathing (SDB) is a common condition and could be a risk factor for cardiovascular morbidity and mortality. However, the pathogenesis of SDB remains to be elucidated. In general, SDB is divided into two forms, obstructive and central sleep apnea (OSA and CSA, respectively). ⋯ CSA primarily results from a fall in PaCO2 to a level below the apnea threshold during sleep through the reflex inhibition of central respiratory drive. It has been reported that UA alterations (i.e., collapse or dilation) can be observed in CSA. This review highlights the roles of the UA in the pathogenesis and pathophysiology of SDB.
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Fibrotic respiratory diseases severely disrupt lung function and currently have an extremely poor prognosis. This is attributable to the limited amount of treatment options available, in part due to our lack of understanding of the mechanisms driving disease pathogenesis. Although the majority of cases appear to be idiopathic, a number of factors are known to cause pulmonary fibrosis, such as the inhalation of silica crystals (silicosis), asbestos fibers (asbestosis) and certain drugs such as bleomycin. ⋯ Moreover, data suggests that inhibition of the inflammasome activation pathway and/or inflammasome-mediated cytokines can attenuate the fibrotic response in in vitro and in vivo models of disease. In this review, we discuss the evidence suggesting that the NLRP3 inflammasome plays an important role in the pathogenesis of fibrotic respiratory diseases, and the potential mechanisms by which activation of the NLRP3 inflammasome may occur. It is possible that fibrotic respiratory diseases with a known cause may share a common mechanism with idiopathic pulmonary fibrosis, providing possible strategies for future drug therapies.