Editorial
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Cardiol. Aug 26, 2015; 7(8): 449-453
Published online Aug 26, 2015. doi: 10.4330/wjc.v7.i8.449
Glycated hemoglobin and its spinoffs: Cardiovascular disease markers or risk factors?
Jumana Saleh
Jumana Saleh, Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat 123, Oman
Author contributions: The editorial was written by the author stated.
Conflict-of-interest statement: No conflict of interest is declared in this invited editorial manuscript.
Open-Access: 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/
Correspondence to: Dr. Jumana Saleh, Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, PO Box 35, Muscat 123, Oman. jumana@squ.edu.om
Telephone: +968-24-143534
Received: February 4, 2015
Peer-review started: February 5, 2015
First decision: April 27, 2015
Revised: May 21, 2015
Accepted: June 9, 2015
Article in press: June 11, 2015
Published online: August 26, 2015
Abstract

Atherosclerosis is a major complication of diabetes, increasing the risk of cardiovascular related morbidities and mortalities. The hallmark of diabetes is hyperglycemia which duration is best predicted by elevated glycated haemoglobin A1C (HbA1C) levels. Diabetic complications are usually attributed to oxidative stress associated with glycation of major structural and functional proteins. This non-enzymatic glycation of long lived proteins such as collagen, albumin, fibrinogen, liver enzymes and globulins result in the formation of early and advanced glycation end products (AGEs) associated with the production of myriads of free radicles and oxidants that have detrimental effects leading to diabetic complications. AGEs have been extensively discussed in the literature as etiological factors in the advancement of atherogenic events. Mechanisms described include the effects of glycation on protein structure and function that lead to defective receptor binding, impairment of immune system and enzyme function and alteration of basement membrane structural integrity. Hemoglobin (Hb) is a major circulating protein susceptible to glycation. Glycated Hb, namely HbA1C is used as a useful tool in the diagnosis of diabetes progression. Many studies have shown strong positive associations between elevated HbA1C levels and existing cardiovascular disease and major risk factors. Also, several studies presented HbA1C as an independent predictor of cardiovascular risk. In spite of extensive reports on positive associations, limited evidence is available considering the role of glycated Hb in the etiology of atherosclerosis. This editorial highlights potential mechanisms by which glycated hemoglobin may contribute, as a causative factor, to the progression of atherosclerosis in diabetics.

Keywords: Glycated hemoglobin, Glycoxidative stress, Advanced glycation end products, Atherosclerosis, Diabetes mellitus

Core tip: Glycated hemoglobin is a useful marker for the diagnosis of diabetes progression. Many studies present glycated haemoglobin (HbA1C) as an independent predictor of cardiovascular risk in diabetics. Although haemoglobin (Hb) is a major circulating protein, limited information is available about the role of glycated Hb as such in the etiology of atherosclerosis. This editorial highlights potential mechanisms by which glycated hemoglobin may contribute, as a causative factor, to the progression of atherosclerosis in diabetics.