Eiras S. Nε-carboxymethyl-lysine and inflammatory cytokines, markers and mediators of coronary artery disease progression in diabetes. World J Diabetes 2024; 15(4): 575-578 [PMID: 38680703 DOI: 10.4239/wjd.v15.i4.575]
Corresponding Author of This Article
Sonia Eiras, BSc, Ph.D., Research Scientist, Senior Researcher, Translational Cardiology, Health Research Institute, University Hospital of Santiago de Compostela, Travesía da Choupana s/n, Santiago de Compostela 15706, Spain. sonia.eiras.penas@sergas.es
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Editorial
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. Apr 15, 2024; 15(4): 575-578 Published online Apr 15, 2024. doi: 10.4239/wjd.v15.i4.575
Nε-carboxymethyl-lysine and inflammatory cytokines, markers and mediators of coronary artery disease progression in diabetes
Sonia Eiras
Sonia Eiras, Translational Cardiology, Health Research Institute, University Hospital of Santiago de Compostela, Santiago de Compostela 15706, Spain
Author contributions: Eiras S contributed to this final scientific letter.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
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 by 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: Sonia Eiras, BSc, Ph.D., Research Scientist, Senior Researcher, Translational Cardiology, Health Research Institute, University Hospital of Santiago de Compostela, Travesía da Choupana s/n, Santiago de Compostela 15706, Spain. sonia.eiras.penas@sergas.es
Received: November 5, 2023 Peer-review started: November 5, 2023 First decision: January 6, 2024 Revised: January 8, 2024 Accepted: March 1, 2024 Article in press: March 1, 2024 Published online: April 15, 2024 Processing time: 159 Days and 0 Hours
Abstract
This editorial refers to the article “Comparative analysis of Nε-carboxymethyl-lysine and inflammatory markers in diabetic and non-diabetic coronary artery disease patients”, published in the recent issue of the World Journal of Diabetes 2023 is based on glucose metabolism, advanced glycation end products (AGEs), inflammation and adiposity on diabetes and coronary artery disease (CAD). This study has included CAD patients who were stratified according to glycosylated hemoglobin higher than 6.5 and sex-matched. A higher prevalence of hypertension, dyslipidemia, and non-vegetarian diet were found in the diabetic group. These risk factors might influence body weight and adiposity and explain the increment of the left atrium. Although this data was not supported by the study. The diet can also explain the non-enzymatic reactions on lipids, proteins, or nucleic acids and consequently an increment of AGEs. These molecules can emit fluorescence. However, one of the non-fluorescent and most abundant AGEs is Nε-carboxymethyl-lysine (CML). Its association with coronary artery stenosis and severity in the diabetic group might suggest its role as a player in CAD progression. Thus, CML, after binding with its receptor (RAGE), can induce calcification cascade through reactive oxygen species and mitogen-activated protein kinase. Moreover, this interaction AGE-RAGE can cause activation of the transcription nuclear factor-kb and induce inflammatory cytokines. It might explain the relationship between CML and pro-inflammatory cytokines in diabetic and CAD patients. Although this is a population from one center, the determination of CML and inflammatory cytokines might improve the diagnosis of severe and progressive CAD. Future and comparative studies among glycosylated hemoglobin, CML, and other AGE levels according to diagnosis and prognosis value might modify the clinical practice. Although these molecules are irreversible, they can act through a specific receptor inducing a signal transduction that might be modu-lated by inhibitors, antibodies, or siRNA. Further mechanistic studies might improve the development of future preventive therapies for diabetic patients.
Core Tip: Coronary artery disease (CAD) is associated with 17.8 million deaths annually and nearly 30% have diabetes with insulin resistance. This metabolic disorder increases the circulating glucose levels that allow the non-enzymatic modifications of proteins, lipids, nucleic acids, etc. and form advanced glycation end products (AGEs). Glycosylated hemoglobin is considered a diagnostic marker for diabetes and a risk factor for CAD. However, AGEs through its receptor (RAGE) might increase signal transduction and consequently, inflammatory cytokines, and endothelial dysfunction and be markers and mediators of CAD.
