Key result
Cardiac-specific overexpression of human IL-1alpha in mice caused concentric left ventricular hypertrophy with preserved left ventricular systolic function.
No immediate clinical implications; leaves open IL-1α's role in human concentric hypertrophy.
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.
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Nishikawa et al. (2006) studied Left ventricular hypertrophy. Cardiac-specific overexpression of human IL-1alpha was evaluated on Heart morphology and functions. Cardiac-specific overexpression of human IL-1alpha in mice caused concentric left ventricular hypertrophy with preserved left ventricular systolic function.
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