Wang ZQ, Yao HP, Sun Z. Nε-(carboxymethyl)lysine promotes lipid uptake of macrophage via cluster of differentiation 36 and receptor for advanced glycation end products. World J Diabetes 2023; 14(3): 222-233 [PMID: 37035231 DOI: 10.4239/wjd.v14.i3.222]
Corresponding Author of This Article
Zhen Sun, PhD, Doctor, Department of Cardiology, Affiliated Hospital of Jiangsu University, No. 438 Jiefang Road, Zhenjiang 212001, Jiangsu Province, China. 1398041019@qq.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Mar 15, 2023; 14(3): 222-233 Published online Mar 15, 2023. doi: 10.4239/wjd.v14.i3.222
Nε-(carboxymethyl)lysine promotes lipid uptake of macrophage via cluster of differentiation 36 and receptor for advanced glycation end products
Zhong-Qun Wang, Hai-Peng Yao, Zhen Sun
Zhong-Qun Wang, Hai-Peng Yao, Zhen Sun, Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China
Author contributions: Sun Z designed the research study; Wang Z and Yao HP performed the research; Wang Z analyzed the data and wrote the manuscript; All authors have read and approve the final manuscript.
Supported byThe National Natural Science Foundation of China, No. 82070455; Natural Science Foundation of Jiangsu Province, No. BK20201225; Medical Innovation Team Project of Jiangsu Province, No. CXTDA2017010.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zhen Sun, PhD, Doctor, Department of Cardiology, Affiliated Hospital of Jiangsu University, No. 438 Jiefang Road, Zhenjiang 212001, Jiangsu Province, China. 1398041019@qq.com
Received: September 22, 2022 Peer-review started: September 22, 2022 First decision: December 26, 2022 Revised: January 8, 2023 Accepted: February 15, 2023 Article in press: February 15, 2023 Published online: March 15, 2023 Processing time: 174 Days and 7.9 Hours
Core Tip
Core Tip: Nε-(carboxymethyl)lysine (CML), a toxic metabolism product in diabetes mellites, is a causative factor of many diseases. CML has been reported to promote lipid uptake in macrophages and foam cell formation. The receptor for advanced glycation end products (RAGE) and cluster of differentiation 36 (CD36) are receptors of CML. However, the roles of RAGE and CD36 in CML-induced lipid uptake in macrophages are currently unclear. Moreover, the relationship and difference between RAGE and CD36 in this process are also worth exploring. The in vitro model was constructed with Raw264.7 cells. Under the stimulation of CML, the lipid uptake by cells was significantly increased. Inhibition of CD36 or RAGE antagonized CML-induced lipid uptake. We synthesized a probe of 18F-CML to explore the relationship of CML to CD36 and to RAGE. CML could bind to CD36 and to RAGE, and CML has a significantly stronger affinity for CD36 than for RAGE. The exploration of the pathogenic mechanism of CML may provide evidence for a deeper understanding of diseases related to metabolic disorders.
