Maurice J P, Koch W J
Department of Surgery and Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Coron Artery Dis. 1999 Sep;10(6):401-5. doi: 10.1097/00019501-199909000-00009.
Congestive heart failure (CHF), despite the improved prevention and treatment modalities adopted for cardiovascular disease over the past two decades, remains a significant therapeutic challenge. Efficacious therapies are few, and death rates from CHF continue to rise. Recent advances in our understanding of the molecular basis of CHF have given rise to experimental animal models demonstrating related genetic phenotypes, which further elucidate cellular mechanisms involved in the pathogenesis of the failing heart. Studies involving transgenic mice have elucidated novel potential gene therapy interventions aimed at the genetic modification of beta-adrenergic signaling in the heart. This review will briefly discuss beta-adrenergic signaling in CHF, while focusing on potential gene therapy strategies to improve the performance of the failing heart.
尽管在过去二十年中针对心血管疾病采用了改进的预防和治疗方式，但充血性心力衰竭（CHF）仍然是一项重大的治疗挑战。有效的治疗方法很少，而且CHF的死亡率持续上升。我们对CHF分子基础认识的最新进展催生了展示相关基因表型的实验动物模型，这进一步阐明了衰竭心脏发病机制中涉及的细胞机制。涉及转基因小鼠的研究阐明了旨在对心脏β-肾上腺素能信号进行基因修饰的新型潜在基因治疗干预措施。本综述将简要讨论CHF中的β-肾上腺素能信号，同时重点关注改善衰竭心脏功能的潜在基因治疗策略。
