GRK 754: Myocardial Gene Expression und Function - Myocardial Hypertrophy

GRK 754：心肌基因表达和功能 - 心肌肥大

• 批准号: 273389
• 金额: --
• 依托单位: Freie Universität Berlin
• 依托单位国家: 德国
• 项目类别: Research Training Groups
• 财政年份: 2001
• 资助国家: 德国
• 起止时间: 2000-12-31 至 2009-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/273389?language=en
• 关键词: GRK; 754; Myocardial; Gene; Expression

Heart failure represents one of the most prominent cardiac problems of all western societies. In most cases it is preceded by myocardial hypertrophy which develops following cardiac overload in hypertension or after myocardial infarction and is frequently associated with old age. Mechanical overload leads to an augmented growth response of the affected cardiac muscle which includes changes in myocardial gene expression. In varying time intervals after development of hypertrophy, remodeling and contractile failure of the hypertrophied myocardium result. The physiological and molecular basis of this development are as yet unclear';' genetic determinants probably play a role. The research aim of the research training grouop is to elucidate the physiological, biochemical and genetic mechanisms that lead to myocardial hypertrophy and its transition into cardiac failure. Better understanding of these mechanisms will create new therapeutic options.

心力衰竭是所有西方社会最突出的心脏问题之一。在大多数情况下，心肌肥大发生在高血压或心肌梗死后的心脏负荷过重之后，通常与老年有关。机械负荷导致受影响心肌的生长反应增强，其中包括心肌基因表达的变化。在不同的时间间隔肥厚发生后，肥厚心肌的重塑和收缩衰竭的结果。这种发展的生理和分子基础尚不清楚；“基因决定因素可能起了作用。研究训练组的研究目的是阐明导致心肌肥厚并向心力衰竭转变的生理、生化和遗传机制。更好地了解这些机制将创造新的治疗选择。