Abstract 13717: Dietary Iron Restriction Attenuates the Development of Left Ventricular Remodeling After Myocardial Infarction in Mice
Background: Iron plays a crucial role in the pathogenesis of several cardiovascular diseases. However the preventive effects of iron restriction (IR) against cardiovascular disease remain incompletely explored. Here, we investigated the impact of dietary IR on left ventricular (LV) remodeling in a mouse model of myocardial infarction (MI).
Methods and Results: MI was induced in male C57BL/6J mice (9 to 11 weeks of age) by ligating the left anterior descending coronary artery. After 14 days surgery, MI mice were randomly divided into untreated (MI) and dietary iron-restricted (MI+IR) groups. Sham operation without ligating the coronary artery was also performed as controls.
Results: MI mice exhibited increased heart weight/tibial length (TL) ratio and left ventricular weight/TL ratio, as compared with the control at day 28 after MI. In contrast, iron restriction attenuated LV hypertrophy. In addition, histological analysis showed increased myocardial fibrosis in the remote myocardium of MI mice, whereas iron restriction suppressed myocardial fibrosis, along with decreased collagen I gene expression. LV fractional shortening was decreased and left ventricular end-diastolic and end-systolic ventricular dimensions was increased on echocardiography in MI mice compared with the control, whereas iron restriction tended to attenuate these changes. Moreover, lung weight/TL ratio was increased in MI mice at day 28 after MI, while iron restriction suppressed this increment. Importantly, gene expression of cellular iron transport proteins, transferrin receptor 1 and divalent metal transporter 1 was increased in the remote myocardium of MI mice compared with the controls. Moreover, a key regulator of iron homeostasis, hepcidin gene expression was increased in the remote myocardium of MI mice.
Conclusions: Iron restriction attenuated the development of LV remodeling after MI. Cellular iron transport might play a role in the pathophysiological mechanism of LV remodeling after MI.
- © 2013 by American Heart Association, Inc.