Intercellular adhesion molecule-1 (ICAM-1) is a member of an immunoglobulin-like 
superfamily of adhesion molecules that mediate leukocyte adhesion to vascular 
endothelium and are involved in several cardiovascular diseases, including 
ischemia-reperfusion injury, myocardial infarction, and atherosclerosis. 
However, the role of ICAM-1 in angiotensin II (ANG II)-induced cardiac 
remodeling in mice remains unclear. Wild-type mice were administered an IgG 
control or ICAM-1 neutralizing antibody (1 and 2 mg/mouse, respectively) and ANG 
II (1,000 ng·kg-1·min-1) for up to 14 days. Cardiac contractile function and 
structure were detected by echocardiography. Hypertrophy, fibrosis, and 
inflammation were assessed by histological examination. The infiltration of 
lymphocyte function-associated antigen-1 (LFA-1+) monocytes/macrophages was 
assessed by immunostaining. The mRNA expression of genes was evaluated by 
quantitative RT-PCR analysis. Protein levels were tested by immunoblotting. We 
found that ICAM-1 expression in ANG II-infused hearts and ICAM-1 levels in serum 
from human patients with heart failure were significantly increased. Moreover, 
ANG II infusion markedly enhanced ANG II-induced hypertension, caused cardiac 
contractile dysfunction, and promoted cardiac hypertrophy, fibrosis, and LFA-1+ 
macrophage infiltration. Conversely, blockage of ICAM-1 with a neutralizing 
antibody dose-dependently attenuated these effects. Moreover, our in vitro data 
further demonstrated that blocking ICAM-1 inhibited ANG II-induced LFA-1+ 
macrophage adhesion to endothelial cells and migration. In conclusion, these 
results provide novel evidence that blocking ICAM-1 exerts a protective effect 
in ANG II-induced cardiac remodeling at least in part through the modulation of 
adhesion and infiltration of LFA-1+ macrophages in the heart. Inhibition of 
ICAM-1 may represent a new therapeutic approach for hypertrophic heart 
diseases.NEW & NOTEWORTHY Leukocyte adhesion to vascular endothelium is a 
critical step in cardiovascular diseases. ICAM-1 is a member of 
immunoglobulin-like superfamily of adhesion molecules that binds LFA-1 to 
mediate leukocytes adhesion and migration. However, the significance of ICAM-1 
in ANG II-induced cardiac remodeling remains unclear. This study reveals that 
blocking of ICAM-1 prevents ANG II-induced cardiac remodeling via modulating 
adhesion and migration of LFA-1+ monocytes, may serve as a novel therapeutic 
target for hypertensive cardiac diseases.