Protein Glycation: A Firm Link to Endothelial Cell Dysfunction

By J. Wautier, A. M. Schmidt. Circulation Research, 2004

825 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/1f557665d5a63514ed76974b12fc5531f66587ea

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1. Yue Liu
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Citations in the corpus

• Diabetic vascular diseases: molecular mechanisms and therapeutic strategies (2023, background): “diaphanous-related 1 (DIAPH 1), ERK1, ERK2, and PKC.(451,453) AGE/ RAGE on mononuclear macrophages increases CD36 expression, promotes OX-LDL uptake while decreasing high-density lipoprotein (HDL) efflux, and promotes foam cell formation; AGE/RAGE action on vascular smooth muscle cells (VSMC) induce”
• Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives (2022, background): “The AGEs/RAGE interaction triggers several signaling cascades such as IKK/NF-κB, ERK/MAPK, PKC, JNK and JAK/STAT and activates transcription factors such as NFκB, CREB, AP-1, and STAT3, which results in oxidative stress and amplifies inflammatory responses.”