Inflammatory markers, oxidative stress, and mitochondrial dynamics: Repercussions on coronary artery disease in diabetes

doi:10.4239/wjd.v15.i9.1853

Advanced Search

BPG is committed to discovery and dissemination of knowledge

Home / Archive / Volume 15, Issue 9

This Article

Academic Content and Language Evaluation of This Article

CrossCheck and Google Search of This Article

Academic Rules and Norms of This Article

Citation of this article

Corresponding Author of This Article

Research Domain of This Article

Article-Type of This Article

Open-Access Policy of This Article

Times Cited Counts in Google of This Article

Number of Hits and Downloads for This Article

Total Article Views (997)

All Articles published online

The chart showing PDF series, WORD series, HTML series, Figures (1-1) series.

Item

Count

PDF

WORD

HTML

730

Figures (1-1)

115

Sum=865

Publishing Process of This Article

The chart showing Browse series, Download series.

Item

Count

Browse

Download

Sum=79

Sep 15, 2024 (publication date) through Dec 1, 2024

Times Cited of This Article

Times Cited (0)

Journal Information of This Article

Publication Name

World Journal of Diabetes

ISSN

1948-9358

Publisher of This Article

Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Editorial

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

Core Tip

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.