Absence of the calcium-binding protein, S100A1, confers pulmonary hypertension in mice associated with endothelial dysfunction and apoptosis

Conclusion
Our data demonstrate that the absence of S100A1 results in PH by disruption of its normal capacity to (i) enhance pulmonary EC function by induction of eNOS activity and NO levels via Akt/ERK1/2 pathways and (ii) promote EC survival. The ability of exogenously administered S100A1 to rescue this phenotype makes it an attractive therapeutic target in the treatment of PH.

Source: Cardiovascular Research - December 26, 2014 Category: Cardiology Authors: Teichert-Kuliszewska, K., Tsoporis, J. N., Desjardins, J.-F., Yin, J., Wang, L., Kuebler, W. M., Parker, T. G. Tags: Integrative physiology and pathophysiology Source Type: research