Does rAGE modulate hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways?
These data illustrate key roles for RAGE-ligand interaction in the pathogenesis of cardiomyocyte injury induced by hypoxia/reoxygenation and indicate that the effects of RAGE are mediated by JNK activation and dephosphorylation of GSK-3beta. The outcome in this study lends further support to the potential use of RAGE blockade as an adjunctive therapy for protection of the ischemic heart.
The analysis did not consider adverse events, and included only five major smoking-related diseases, which is a conservative approach, and probably leads to under-estimation of cost-effectiveness of cessation interventions. Furthermore, assumptions of constant relative risks for smoking-related diseases for each smoking status and the proxy values used as efficacy estimates of second quit attempts for other interventions than varenicline are limitations.