Key result
RAGE silencing attenuates prothrombogenic macrophage regulation in hyperlipidemic rabbits independent of diabetes.
Why the study?
While the AGE/RAGE axis plays a central role in diabetic vascular remodeling, its role in nondiabetic atherosclerosis remained to be clarified.
Population
Aortic and coronary atherosclerotic lesions of WHHLMI rabbits at 1 to 14 months, plus macrophage cell lines
Comparison
RAGE expression across age groups and RAGE silencing vs control in vitro
Design
Preclinical animal and in vitro laboratory study
Authors
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Hypothesis-generating for RAGE as a target in nondiabetic atherosclerosis; animal data leave clinical translation unresolved.
RAGE plays an integral role in the initiation and progression of nondiabetic atherosclerosis, suggesting it may be a novel therapeutic target for nondiabetic vascular complications.
Uekita et al. (2019) studied Nondiabetic atherosclerosis. RAGE expression and silencing was evaluated on RAGE expression, AGE accumulation, and prothrombogenic molecular regulation. RAGE expression is induced by hyperlipidemia and oxidative stress independent of diabetes in WHHLMI rabbits, and its silencing attenuates prothrombogenic molecular regulation in macrophages.
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