Exposure to Humidifier Disinfectants Increases the Risk for Asthma in Children

across the genome, including pathways highly relevant to PAH pathogenesis, such as WNT signaling (8, 10,11).One of the findings in our study was that the positive effect of SRY on BMPR2 expression had an upper limit, above which adding more SRY did not result in a corresponding increase in BMPR2 expression.This is not a surprising finding, as most transcription factors have a limited range of function.Furthermore, BMPR2 expression is likely controlled by a coordinated action of multiple different transcriptional regulators, and thus one transcription factor would not be expected to modify its expression to an unlimited extent.For example, previous studies have identified other factors that regulate BMPR2 expression, such as estrogen receptor a (4, 5).Thus, the integration of multiple factors may explain why SRY has a limited, but important, capacity to increase BMPR2 expression.Each factor may play a role in PAH susceptibility or resilience.It is important to acknowledge that in some assays, the effect sizes were modest; this may reflect the fact that multiple factors likely contribute to BMPR2 expression, not simply SRY activity.Finally, much of this work was conducted using PAH fibroblasts because of the low expression of SRY in typical lung vascular cells.Although the amount of data suggesting that fibroblasts may contribute to PAH pathogenesis is growing, future work will determine whether SRY contributes to variations in lung vascular cell health and function.In conclusion, SRY binds to and positively regulates BMPR2 expression.This builds on recent novel work by Umar and colleagues, which demonstrated the relevance of the Y chromosome to pulmonary hypertension (7).Our findings advance the concept that protective factors on the Y chromosome contribute to pulmonary hypertension, with a focus on the reduced male incidence in PAH via sex-specific BMPR2 regulation.