β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions

Pro-apoptotic effect of anti-β1-adrenergic receptor antibodies in periodontitis patients

“…Alternatively, metoprolol could prevent apoptosis through its action on β adrenergic signaling and its metabolic actions could decrease oxidative stress [35]. Moreover, three β-AR subtypes (β 1 -AR, β 2 -AR, β 3 -AR) are expressed in cardiomyocytes and norepinephrine or isoproterenol stimulated all β-AR and induced apoptosis in rat cardiomyocytes and it is thought that a β 1 -AR-mediated pathway primarily contributes to apoptosis [36,37].…”

“…The mean age was 41 (range, 32-50) years. Healthy subjects were used as controls (15 male subjects) with a mean age of 38 (range, [30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] years. The assessment of clinical parameters was carried out by a trained periodontist following the criteria based on clinical parameters and the severity of periodontal tissue destruction [29].…”

Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection

“…Further work is warranted in unravelling the roles of caveolae and caveolin-3 in control of cardiomyocyte EGFR signalling. Importantly, significant reductions in myocardial caveolin-3 expression/localisation with ageing (Kawabe et al, 2001;Ratajczak et al, 2003;Peart et al, 2007), infarction (Ratajczak et al, 2003), and disease (Piech et al, 2003;Penumathsa et al, 2008;Crossman et al, 2011;Sharma et al, 2011;Lei et al, 2013) have the potential to dysregulate myocardial EGFR signalling.…”

Mechanisms of Lipotoxicity in the Cardiovascular System

“…Pharmacologic inhibition of β-adrenergic receptors with metoprolol in streptozotocin-treated mice inhibited CPT1, but did not prevent cardiac lipid accumulation or oxidative stress. Of note, metoprolol treatment-activated PKB mediated signaling to reduce caspase activation and promote cell survival [84]. Finally, in a recent study in a mouse model of longstanding diet-induced obesity (6 months of 60 % high-fat feeding), cardiac dysfunction was prevented in mice with cardiac-specific deletion of FOXO1, suggesting an important role for nuclear FOXO signaling in mediating obesity and diabetes-related cardiac dysfunction [85•].…”