scholarly journals The Oxidative Stress and Mitochondrial Dysfunction during the Pathogenesis of Diabetic Retinopathy

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Meng-Yu Wu ◽  
Giou-Teng Yiang ◽  
Tzu-Ting Lai ◽  
Chia-Jung Li
Keyword(s):  
Diabetic Retinopathy ◽  
Mitochondrial Dysfunction ◽  
Microvascular Complications ◽  
Microvascular Dysfunction ◽  
Oxygen Species ◽  
Local Inflammation ◽  
Advanced Glycation ◽  
Kinase C ◽  
Glycation End Products

Diabetic retinopathy is one of the most serious microvascular complications induced by hyperglycemiaviafive major pathways, including polyol, hexosamine, protein kinase C, and angiotensin II pathways and the accumulation of advanced glycation end products. The hyperglycemia-induced overproduction of reactive oxygen species (ROS) induces local inflammation, mitochondrial dysfunction, microvascular dysfunction, and cell apoptosis. The accumulation of ROS, local inflammation, and cell death are tightly linked and considerably affect all phases of diabetic retinopathy pathogenesis. Furthermore, microvascular dysfunction induces ischemia and local inflammation, leading to neovascularization, macular edema, and neurodysfunction, ultimately leading to long-term blindness. Therefore, it is crucial to understand and elucidate the detailed mechanisms underlying the development of diabetic retinopathy. In this review, we summarized the existing knowledge about the pathogenesis and current strategies for the treatment of diabetic retinopathy, and we believe this systematization will help and support further research in this area.

scholarly journals Az oxidatív stressz szerepe a diabeteses neuropathia kialakulásában

2016 ◽  
Vol 157 (49) ◽  
pp. 1939-1946 ◽  
Author(s):  
Ferenc Sztanek ◽  
Ágnes Molnárné Molnár ◽  
Zoltán Balogh
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Microvascular Complications ◽  
Advanced Glycation ◽  
Complications Of Diabetes ◽  
Kinase C ◽  
Glycation End Products ◽  
Comparative Trials

Diabetic neuropathy may be one of the most common and severe complications of diabetes mellitus. Oxidative stress plays a pivotal role in the development of microvascular complications of diabetes. The majority of related pathways like polyol and hexosamine, advanced glycation end products, poly-ADP-ribose polymerase, and protein kinase-C all originated from initial oxidative stress. In this review, the authors present the current oxidative stress hypothesis in diabetes mellitus and summarize the pathophysiological mechanisms of diabetic neuropathy associated with increased oxidative stress. The development of modern medicines to treat diabetic neuropathy needs intensive long-term comparative trials in the future. Orv. Hetil., 2016, 157(49), 1939–1946.

Glucose Effects on the Peritoneum: What Can We Learn from Rodent Models?

2012 ◽  
Vol 120 (04) ◽  
pp. 197-198 ◽  
Author(s):  
S. Müller-Krebs ◽  
W. Zhang ◽  
L. Kihm ◽  
J. Reiser ◽  
P. Nawroth ◽  
...  
Keyword(s):  
Vitamin B1 ◽  
Rodent Models ◽  
Peritoneal Membrane ◽  
Advanced Glycation ◽  
Detoxifying Enzymes ◽  
Functional Reorganization ◽  
Glycation End Products ◽  
Glucose Metabolites ◽  
Glucose Effects

AbstractDuring long-term peritoneal dialysis (PD) the peritoneal membrane underlies processes of structural and functional reorganization mediated by high glucose and reactive glucose metabolites that are contained in PD solutions; this process is accompanied by increasing fibrosis. Mechanistically, the peritoneal damage is triggered by the interaction of advanced glycation end-products with their receptor; this is true for rodents as well as for humans. With this knowledge interventional strategies can be tested in rodent models, among them are the lipid soluble vitamin B1 analogue benfotiamine (BF) or detoxifying enzymes such as glyoxalase. Of additional interest is the finding that PD fluids do not only cause local but also systemic damage, in particular renal and cardiovascular. In the case of kidney damage, the intervention with BF was also successful. Taken together, PD can be regarded as a local model for long-term diabetes together with systemic aspects of damage.

scholarly journals Advanced Glycation End Products and Oxidative Stress in a Hyperglycaemic Environment

2021 ◽  
Author(s):  
Akio Nakamura ◽  
Ritsuko Kawahrada
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Advanced Glycation End Products ◽  
Reactive Oxygen ◽  
Protein Glycation ◽  
Oxygen Species ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
And Oxidative Stress

Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.

scholarly journals Advanced Glycation End Products: Formation, Role in Diabetic Complications, and Potential in Clinical Applications

2020 ◽  
Author(s):  
Rujman Khan ◽  
Xin Yee Ooi ◽  
Matthew Parvus ◽  
Laura Valdez ◽  
Andrew Tsin
Keyword(s):  
Diabetic Retinopathy ◽  
Advanced Glycation End Products ◽  
Diabetic Complications ◽  
Tanshinone Iia ◽  
Future Research ◽  
Advanced Glycation ◽  
Reactive Aldehydes ◽  
Glycation End Products ◽  
End Products ◽  
Lysine Residues

Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products (AGEs). These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors (RAGE) on pericytes and Muller cells. Damage occurring between AGE and RAGE potentially generates reactive oxygen species, inflammatory cytokines, and growth factors. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Other pharmaceutical interventions, such as Tanshinone IIA, aim to protect cells from the impacts of AGEs. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.

Carbonyl Stress: Increased Carbonyl Modification of Tissue and Cellular Proteins in Uremia

1999 ◽  
Vol 19 (2_suppl) ◽  
pp. 58-61 ◽  
Author(s):  
Toshio Miyata ◽  
Yuko Izuhara ◽  
Hideto Sakai ◽  
Kiyoshi Kurokawa
Keyword(s):  
Carbonyl Compounds ◽  
Inflammatory Responses ◽  
Surface Proteins ◽  
Matrix Proteins ◽  
Cellular Proteins ◽  
Carbonyl Stress ◽  
Advanced Glycation ◽  
Endothelial Cell Surface ◽  
Glycation End Products

Advanced glycation end-products (AGEs) are formed during non enzymatic glycation and oxidation (glycoxidation) reactions. This process is accelerated in diabetics owing to hyperglycemia, and it has been implicated in the pathogenesis of diabetic complications. Surprisingly, AGEs increase in normoglycemic uremic patients to a much greater extent than in diabetics. AGE accumulation in uremia cannot be attributed to hyperglycemia nor simply to a decreased removal by glomerular filtration. Recently gathered evidence has suggested that, in uremia, the increased carbonyl compounds derived from carbohydrates and lipids modify proteins not only by glycoxidation reaction but also by lipoxidation reaction (“carbonyl stress”). Carbonyl stress has been implicated in the pathogenesis of long-term uremic complications such as dialysisrelated amyloidosis. With regard to continuous ambulatory peritoneal dialysis (CAPD), the peritoneal cavity appears to be in a state of severe overload of carbonyl compounds derived from CAPD solution containing high glucose, from heat sterilization of the solution, and from uremic circulation. Carbonyl stress might modify not only peritoneal matrix proteins and alter their structures, but also react with mesothelial and endothelial cell surface proteins and initiate a range of inflammatory responses. Carbonyl stress might therefore contribute to the development of peritoneal sclerosis in patients with long-term CAPD.

Sign in / Sign up

Export Citation Format

Share Document