Soluble RAGE significantly attenuated Angiotensin II-induced left ventricular hypertrophy in mice, reducing end-diastolic myocardial weight compared to AngII alone.
Does sRAGE attenuate AngII-induced left ventricular hypertrophy in a mouse model?
sRAGE significantly attenuates AngII-induced left ventricular hypertrophy in mice, as assessed by high-field in vivo MRI.
Absolute Event Rate: 105.8% vs 118%
p-value: p=<0.05
We investigated the effectiveness of soluble Receptor for Advanced Glycation Endproducts (sRAGE) in attenuating angiotensin II (AngII)-induced left ventricular hypertrophy (LVH) using in vivo 9.4T cine-magnetic resonance imaging (CINE-MRI). Mice were divided into four groups: AngII (n = 9), saline (n = 10), sRAGE (n = 10), and AngII + sRAGE (n = 10). CINE-MRI was performed in each group after administration of the AngII or sRAGE, and CINE-MR images were analyzed to obtain parameters indicating cardiac anatomical and functional changes including end-diastolic and end-systolic blood volume, end-diastolic and end-systolic myocardial volume, ejection fraction, end-diastolic and end-systolic myocardial mass, and LV wall thickness. LVH observed in AngII group was significantly attenuated by sRAGE. These trends were also observed in histological analysis, demonstrating that cardiac function tracking using in vivo and real-time 9.4T MR imaging provides valuable information about the cardiac remodeling induced by AngII and sRAGE in an AngII-induced LV hypertrophy mice model.
Heo et al. (Tue,) conducted a other in Angiotensin II-induced left ventricular hypertrophy (n=39). soluble RAGE (sRAGE) vs. Angiotensin II alone was evaluated on End-diastolic myocardial weight (EDmw) in mg (p=<0.05). Soluble RAGE significantly attenuated Angiotensin II-induced left ventricular hypertrophy in mice, reducing end-diastolic myocardial weight compared to AngII alone.