Takotsubo cardiomyopathy (also referred to as transient apical ballooning syndrome, broken heart syndrome or stress cardiomyopathy) is an increasingly recognized entity in the western world typically characterized by ...Takotsubo cardiomyopathy (also referred to as transient apical ballooning syndrome, broken heart syndrome or stress cardiomyopathy) is an increasingly recognized entity in the western world typically characterized by reversible left ventricular dysfunction that develops in the setting of acute severe emotional or physical stress. Increased catecholamine levels have been proposed to play a central role in the pathogenesis of the disease, although the specific pathophysiology of this condition remains elusive at the present moment. In recent times, there have been reports of takotsubo cardiomyopathy (TC) following medical interventions such as invasive or surgical procedures or specific medical regimens. In the current report, we present a patient with multiple recurrences of TC triggered by the same medical therapeutic intervention; in our particular case, repetitive exposure to inhaled beta-2-adrenoceptor agonist.展开更多
β3-adrenoceptor（β3-AR） has been shown to promote myocardial apoptosis. However, the exact physiological role and importance of this receptor in the human myocardium, and its underlying mode of action, have not bee...β3-adrenoceptor（β3-AR） has been shown to promote myocardial apoptosis. However, the exact physiological role and importance of this receptor in the human myocardium, and its underlying mode of action, have not been fully elucidated. The present study aimed to determine the effects of β3-AR on the promotion of myocardial apoptosis and on norepinephrine（NE） injury. We analyzed NE-induced cardiomyocyte（CM） apoptosis by using a TUNEL and an annexin V/propidium iodide apoptosis assay. Furthermore, we investigated the NE-induced expression of the apoptosis marker genes Akt and p38 MAPK, their phosphorylated counterparts p-Akt and p-p38 MAPK, caspase-3, Bcl-2, and Bax. In addition, we determined the effect of a 48-h treatment with a β3-AR agonist and antagonist on expression of these marker genes. β3-AR overexpression was found to increase CM apoptosis, accompanied by an increased expression of caspase-3, bax/bcl-2, and p-p38 MAPK. In contrast, the β3-blocker reduced apoptosis of CMs and the associated elevated Akt expression. We identified a novel and potent anti-apoptosis mechanism via the PI3K/Akt pathway and a pro-apoptosis pathway mediated by p38 MAPK.展开更多
文摘Takotsubo cardiomyopathy (also referred to as transient apical ballooning syndrome, broken heart syndrome or stress cardiomyopathy) is an increasingly recognized entity in the western world typically characterized by reversible left ventricular dysfunction that develops in the setting of acute severe emotional or physical stress. Increased catecholamine levels have been proposed to play a central role in the pathogenesis of the disease, although the specific pathophysiology of this condition remains elusive at the present moment. In recent times, there have been reports of takotsubo cardiomyopathy (TC) following medical interventions such as invasive or surgical procedures or specific medical regimens. In the current report, we present a patient with multiple recurrences of TC triggered by the same medical therapeutic intervention; in our particular case, repetitive exposure to inhaled beta-2-adrenoceptor agonist.
基金supported by the National Natural Science Foundation of China(No.81260028)
文摘β3-adrenoceptor（β3-AR） has been shown to promote myocardial apoptosis. However, the exact physiological role and importance of this receptor in the human myocardium, and its underlying mode of action, have not been fully elucidated. The present study aimed to determine the effects of β3-AR on the promotion of myocardial apoptosis and on norepinephrine（NE） injury. We analyzed NE-induced cardiomyocyte（CM） apoptosis by using a TUNEL and an annexin V/propidium iodide apoptosis assay. Furthermore, we investigated the NE-induced expression of the apoptosis marker genes Akt and p38 MAPK, their phosphorylated counterparts p-Akt and p-p38 MAPK, caspase-3, Bcl-2, and Bax. In addition, we determined the effect of a 48-h treatment with a β3-AR agonist and antagonist on expression of these marker genes. β3-AR overexpression was found to increase CM apoptosis, accompanied by an increased expression of caspase-3, bax/bcl-2, and p-p38 MAPK. In contrast, the β3-blocker reduced apoptosis of CMs and the associated elevated Akt expression. We identified a novel and potent anti-apoptosis mechanism via the PI3K/Akt pathway and a pro-apoptosis pathway mediated by p38 MAPK.
