Nishikawa Kenichiro, Yoshida Mikoto, Kusuhara Masatoshi, Ishigami Norio, Isoda Kikuo, Miyazaki Kohji, Ohsuzu Fumitaka
Internal Medicine-1, National Defense Medical College, 3-2 Namiki Tokorozawa Saitama, 359-0042, Japan.
Am J Physiol Heart Circ Physiol. 2006 Jul;291(1):H176-83. doi: 10.1152/ajpheart.00269.2005. Epub 2006 Feb 10.
Recent studies have identified the importance of proinflammatory cytokines in the development of left ventricular (LV) hypertrophy. However, the precise role of interleukin-1 (IL-1), one of the major proinflammatory cytokines, in the myocardium is not fully understood. In this study, we investigated the pathophysiological consequences of cardiac expression of IL-1 in vivo. We generated mice with a cardiac-specific overexpression of human IL-1alpha. We then analyzed their heart morphology and functions. Histological and echocardiographic analyses revealed concentric LV hypertrophy with preserved LV systolic function in the mice. Our results suggest that myocardial expression of IL-1 is sufficient to cause LV hypertrophy.
最近的研究已经确定促炎细胞因子在左心室（LV）肥厚发展中的重要性。然而，主要促炎细胞因子之一白细胞介素-1（IL-1）在心肌中的精确作用尚未完全明确。在本研究中，我们在体内研究了心脏表达IL-1的病理生理后果。我们构建了心脏特异性过表达人IL-1α的小鼠。然后我们分析了它们的心脏形态和功能。组织学和超声心动图分析显示这些小鼠出现向心性LV肥厚且LV收缩功能保留。我们的结果表明，心肌中IL-1的表达足以导致LV肥厚。
