Association of dietary iron restriction with left ventricular remodeling after myocardial infarction in mice
Akiyo Eguchi1, Yoshiro Naito2, Toshihiro Iwasaku1
1Cardiovascular Division, Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, 663-8501, Japan.
Abstract:
Several epidemiologic studies have reported that body iron status and dietary iron intake are related to an increased risk of acute myocardial infarction (MI). However, it is completely unknown whether dietary iron reduction impacts the development of left ventricular (LV) remodeling after MI. Here, we investigate the effect of dietary iron restriction on the development of LV remodeling after MI in an experimental model. MI was induced in C57BL/6 J mice (9-11 weeks of age) by the permanent ligation of the left anterior descending coronary artery (LAD). At 2 weeks after LAD ligation, mice were randomly divided into two groups and were given a normal diet or an iron-restricted diet for 4 weeks. Sham operation without LAD ligation was also performed as controls. MI mice exhibited increased LV dilatation and impaired LV systolic function that was associated with cardiomyocyte hypertrophy and interstitial fibrosis in the remote area, as compared with the controls at 6 weeks after MI. In contrast, dietary iron restriction attenuated LV dilatation and impaired LV systolic function coupled to cardiomyocyte hypertrophy and interstitial fibrosis in the remote area. Importantly, cardiac expression of cellular iron transport proteins, transferrin receptor 1 and divalent metal transporter 1 was increased in the remote area of MI mice compared with the controls. Dietary iron restriction attenuated the development of LV remodeling after MI in mice. Cellular iron transport might play a role in the pathophysiological mechanism of LV remodeling after MI.
Insights
Dietary iron restriction attenuated adverse left ventricular (LV) remodeling and improved systolic function after myocardial infarction (MI) in mice. This suggests cellular iron transport plays a role in post-MI cardiac dysfunction.
Area of Science:
- Cardiovascular Research
- Iron Metabolism
- Cardiac Pathophysiology
Background:
- Epidemiologic studies link body iron status and dietary iron intake to increased risk of acute myocardial infarction (MI).
- The impact of dietary iron reduction on left ventricular (LV) remodeling post-MI remains unexplored.
Purpose of the Study:
- To investigate the effect of dietary iron restriction on the development of LV remodeling following MI in an experimental mouse model.
Main Methods:
- Myocardial infarction (MI) was induced in C57BL/6 J mice via permanent ligation of the left anterior descending coronary artery (LAD).
- Mice received either a normal or iron-restricted diet for 4 weeks post-MI.
- Sham-operated mice served as controls.
Main Results:
- MI mice showed increased LV dilatation, impaired systolic function, cardiomyocyte hypertrophy, and interstitial fibrosis compared to controls.
- Dietary iron restriction significantly attenuated these adverse LV remodeling changes.
- Cardiac expression of iron transport proteins (TfR1, DMT1) was elevated in MI mice and reduced by iron restriction.
Conclusions:
- Dietary iron restriction mitigates adverse LV remodeling and functional impairment after MI in mice.
- Cellular iron transport mechanisms are implicated in the pathophysiology of post-MI LV remodeling.
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