Basic mechanisms of myocardial dysfunction: cellular pathophysiology of heart failure.
Basic mechanisms of myocardial dysfunction: cellular pathophysiology of heart failure.
复制标题
心肌功能障碍的基本机制：心力衰竭的细胞病理生理学。
DOI：
10.1097/00001573-199505000-00003
复制
发表时间：
1995
影响因子：
2.3
通讯作者：
Camacho,SA
中科院分区：
文献类型：
--
作者：
Figueredo,VM;Camacho,SA
1994年发表的许多研究大大增加了我们在细胞和亚细胞水平上对心力衰竭的病理生理学的理解。这一领域使用不同但互补的方法继续向前推进。一种方法是研究人类心肌，从而提供与临床疾病直接相关的数据。另一种方法是研究小鼠心肌，利用转基因技术改变基因表达，直接研究因果关系。此外，心力衰竭的其他动物模型(例如，压力超负荷、容量超负荷和起搏性心动过速)继续提供重要信息。钙循环、肌丝对钙的敏感性、跨桥动力学、肌细胞骨架和能量学的异常都在动物模型或衰竭的人类心肌中观察到。这些异常的细胞和分子基础目前正在探索中。这种理解对于开发新的治疗策略至关重要，这些策略有朝一日可能包括基因疗法。
Many studies published in 1994 significantly added to our understanding of the pathophysiology of heart failure at the cellular and subcellular level. This field continues to advance using different but complementary approaches. One approach is to study human myocardium, thereby providing data that is directly relevant to clinical disease. Another approach is to study mouse myocardium, taking advantage of transgenic technology to alter gene expression and directly study cause-and-effect relationships. Additionally, other animal models of heart failure (eg, pressure overload, volume overload, and paced tachycardia) continue to provide important information. Abnormalities of calcium cycling, myofilament sensitivity to calcium, cross-bridge kinetics, the myocyte cytoskeleton, and energetics have all been observed in animal models or failing human myocardium. The cellular and molecular basis for these abnormalities is now being explored. This understanding is essential for developing novel treatment strategies that may one day include gene therapy.