Advanced Glycation End Products Induce Atherosclerosis via RAGE/TLR4 Signaling Mediated-M1 Macrophage Polarization-Dependent Vascular Smooth Muscle Cell Phenotypic Conversion

Objective. The objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS). Methods. Toll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrop...

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Veröffentlicht in:	Oxidative medicine and cellular longevity 2022, Vol.2022, p.9763377-11
Hauptverfasser:	Xing, Yujie, Pan, Shuo, Zhu, Ling, Cui, Qianwei, Tang, Zhiguo, Liu, Zhongwei, Liu, Fuqiang
Format:	Artikel
Sprache:	eng
Schlagworte:	Age Animals Antibiotics Atherosclerosis Atherosclerosis - genetics Diabetes Glycation End Products, Advanced - metabolism Humans Kinases Macrophages - metabolism Male Metabolites Mice Phenotype Signal Transduction Smooth muscle Toll-Like Receptor 4 - metabolism Transfection
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