Schiattarella Gabriele Giacomo, Perrino Cinzia, Gargiulo Giuseppe, Sorrentino Sabato, Franzone Anna, Capretti Giuliana, Esposito Giovanni, Chiariello Massimo
Cattedra di Cardiologia, Dipartimento Universitario di Medicina Clinica, Scienze Cardiovascolari ed Immunologiche, Università degli Studi Federico II, Napoli.
G Ital Cardiol (Rome). 2010 Mar;11(3):221-8.
Heart failure is a common and complex clinical syndrome characterized by progressive ventricular dilatation, depressed contractile function and premature death. Abnormalities in the beta-adrenergic receptor (betaAR) signaling such as betaAR down-regulation and desensitization are hallmarks of heart failure. Results from previous studies suggest that chronic betaAR dysfunction in the failing heart is maladaptive and contributes to the deterioration in cardiac function. In this review we will discuss a number of recent studies on betaAR signaling and addressing the role of phosphoinositide-3 kinase (PI3K) in the development of betaAR dysfunction and the progression of heart failure. Novel possible strategies to ameliorate cardiac dysfunction in heart failure through the competitive inhibition of PI3K are also described.
心力衰竭是一种常见且复杂的临床综合征,其特征为进行性心室扩张、收缩功能降低和过早死亡。β-肾上腺素能受体(βAR)信号传导异常,如βAR下调和脱敏,是心力衰竭的标志。先前研究结果表明,衰竭心脏中的慢性βAR功能障碍具有不良适应性,并导致心脏功能恶化。在本综述中,我们将讨论一些关于βAR信号传导的最新研究,并探讨磷酸肌醇-3激酶(PI3K)在βAR功能障碍发展和心力衰竭进展中的作用。还描述了通过竞争性抑制PI3K来改善心力衰竭心脏功能障碍的新型可能策略。