血管生成
心肌细胞
肌肉肥大
医学
心力衰竭
内科学
心肌细胞
心功能曲线
容量过载
串扰
心脏病学
生物
细胞生物学
压力过载
心肌肥大
物理
光学
作者
Tôru Oka,Hiroshi Akazawa,Atsuhiko T. Naito,Issei Komuro
出处
期刊:Circulation Research
[Ovid Technologies (Wolters Kluwer)]
日期:2014-01-31
卷期号:114 (3): 565-571
被引量:346
标识
DOI:10.1161/circresaha.114.300507
摘要
Cardiac hypertrophy is an adaptive response to physiological and pathological overload. In response to the overload, individual cardiac myocytes become mechanically stretched and activate intracellular hypertrophic signaling pathways to re-use embryonic transcription factors and to increase the synthesis of various proteins, such as structural and contractile proteins. These hypertrophic responses increase oxygen demand and promote myocardial angiogenesis to dissolve the hypoxic situation and to maintain cardiac contractile function; thus, these responses suggest crosstalk between cardiac myocytes and microvasculature. However, sustained pathological overload induces maladaptation and cardiac remodeling, resulting in heart failure. In recent years, specific understanding has increased with regard to the molecular processes and cell-cell interactions that coordinate myocardial growth and angiogenesis. In this review, we summarize recent advances in understanding the regulatory mechanisms of coordinated myocardial growth and angiogenesis in the pathophysiology of cardiac hypertrophy and heart failure.
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