Editorial
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Sep 15, 2024; 15(9): 1853-1857
Published online Sep 15, 2024. doi: 10.4239/wjd.v15.i9.1853
Inflammatory markers, oxidative stress, and mitochondrial dynamics: Repercussions on coronary artery disease in diabetes
José Carlos Tatmatsu-Rocha, Luan Santos Mendes-Costa
José Carlos Tatmatsu-Rocha, College of Medicine, Postgraduate Program in Physiotherapy and Functionality, Federal University of Ceará-UFC, Fortaleza 60430-450, Ceará, Brazil
Luan Santos Mendes-Costa, Physical Therapy, Federal University of Ceará, Fortaleza 60000-000, Ceará, Brazil
Author contributions: Tatmatsu-Rocha JC and Mendes-Costa LS contributed to this article; Tatmatsu-Rocha JC designed the overall concept and draft of the manuscript; Mendes-Costa LS contributed to the discussion and conception of the manuscript; Both authors contributed to writing and editing the manuscript and literature review.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
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: José Carlos Tatmatsu-Rocha, MSc, PhD, Professor, Research Scientist, College of Medicine, Postgraduate Program in Physiotherapy and Functionality, Federal University of Ceará-UFC, 1127 Coronel Nunes de Melo, Fortaleza 60430-450, Ceará, Brazil. tatmatsu@ufc.br
Received: April 3, 2024
Revised: May 11, 2024
Accepted: May 31, 2024
Published online: September 15, 2024
Processing time: 146 Days and 1.8 Hours
Abstract

Inflammatory markers and mediators that affect the development of car-diovascular diseases have been the focus of recent scientific work. Thus, the purpose of this editorial is to promote a critical debate about the article titled “Nε-carboxymethyl-lysine and inflammatory cytokines, markers, and mediators of coronary artery disease progression in diabetes”, published in the World Journal of Diabetes in 2024. This work directs us to reflect on the role of advanced glycation end products, which are pro-inflammatory products arising from the metabolism of fatty acids and sugars whose main marker in tissues is Nε-carboxymethyl-lysine (NML). Recent studies have linked high levels of pro-inflammatory agents with the development of coronary artery disease (CAD), especially tumor necrosis factor alpha, interleukins, and C-reactive protein. These inflammatory agents increase the production of reactive oxygen species (ROS), of which people with diabetes are known to have an increased production. The increase in ROS promotes lipid peroxidation, which causes damage to myocytes, promoting myocardial damage. Furthermore, oxidative stress induces the binding of NML to its receptor RAGE, which in turn activates the nuclear factor-kB, and conse-quently, inflammatory cytokines. These inflammatory cytokines induce endo-thelial dysfunction, with increased expression of adhesion molecules, changes in endothelial permeability and changes in the expression of nitric oxide. In this sense, the therapeutic use of monoclonal antibodies (inflammatory reducers such as statins and sodium-glucose transport inhibitors) has demonstrated positive results in the regression of atherogenic plaques and consequently CAD. On the other hand, many studies have demonstrated a relationship between mito-chondrial dynamics, diabetes, and cardiovascular diseases. This link occurs since ROS have their origin in the imbalance in glucose metabolism that occurs in the mitochondrial matrix, and this imbalance can have its origin in inadequate diet as well as some pathologies. Photobiomodulation (PBM) has recently been considered a possible therapeutic agent for cardiovascular diseases due to its effects on mitochondrial dynamics and oxidative stress. In this sense, therapies such as PBM that act on pro-inflammatory mediators and mitochondrial modulation could benefit those with cardiovascular diseases.

Keywords: Mitochondrial dynamics; Diabetes; Oxidative stress; Coronary artery disease; Nε-carboxymethyl-lysine

Core Tip: Increased oxidative stress promoted by pro-inflammatory mediators such as Nε-carboxymethyl-lysine causes changes in mitochondrial dynamics and has been associated with insulin resistance and cardiovascular diseases. Therapies that promote the health of mitochondria by balancing the mechanisms of mitochondrial fusion and fission may be a path forward in the context of coronary artery disease.