Gupta Sudhiranjan, Das Biswajit, Sen Subha
Department of Molecular Cardiology, Lerner Research Institute, The Cleveland Clinic, Cleveland, Ohio 44195, USA.
Antioxid Redox Signal. 2007 Jun;9(6):623-52. doi: 10.1089/ars.2007.1474.
Cardiac hypertrophy and heart failure are major causes of morbidity and mortality in Western societies. Many factors have been implicated in cardiac remodeling, including alterations in gene expression in myocytes, cardiomyocytes apoptosis, cytokines and growth factors that influence cardiac dynamics, and deficits in energy metabolism as well as alterations in cardiac extracellular matrix composition. Many therapeutic means have been shown to prevent or reverse cardiac hypertrophy. New concepts for characterizing the pathophysiology of cardiac hypertrophy have been drawn from various aspects, including medical therapy and gene therapy, or use of stem cells for tissue regeneration. In this review, we focus on various types of cardiac hypertrophy, defining the causes of hypertrophy, describing available animal models of hypertrophy, discussing the mechanisms for development of hypertrophy and its transition to heart failure, and presenting the potential use of novel promising therapeutic strategies derived from new advances in basic scientific research.
心脏肥大和心力衰竭是西方社会发病和死亡的主要原因。许多因素与心脏重塑有关,包括心肌细胞基因表达的改变、心肌细胞凋亡、影响心脏动力学的细胞因子和生长因子、能量代谢缺陷以及心脏细胞外基质组成的改变。许多治疗方法已被证明可预防或逆转心脏肥大。从医学治疗、基因治疗或使用干细胞进行组织再生等各个方面,已经得出了表征心脏肥大病理生理学的新概念。在本综述中,我们重点关注各种类型的心脏肥大,确定肥大的原因,描述现有的肥大动物模型,讨论肥大发展及其向心力衰竭转变的机制,并介绍源自基础科学研究新进展的新型有前景治疗策略的潜在用途。