Does endocardial Endothelial Dysfunction Progressively disrupt Initially Anti then Pro-Thrombotic Pathways in Heart Failure Mice?
CREBA133 mice develop HF and endocardial endothelial dysfunction. Attenuation of the anti-coagulant APC pathway promotes endocardial thrombosis in early and acute decompensated phases of HF. However, in stable compensated HF mice, disruptions in endothelial vWF expression and extrusion may actually reduce the incidence of endocardial thrombosis.
Our results indicate that APE1 is a new promising target for the combination of cisplatin-based chemotherapy in NCSLC patients.