Targeting the receptor for advanced glycation end products (RAGE) in type 1 diabetes

Bagge, Selena Le; Fotheringham, Amelia K.; Leung, Sherman S.; Forbes, Josephine M.

doi:10.1002/med.21654

Cited by 38 publications

(32 citation statements)

References 199 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chronic hyperglycemia, frequently observed in experimental models and human diabetes, exhibits elevated AGE formation, serum AGE levels, RAGE expression, and AGE-RAGE interactions. Consequently, these changes lead to increased oxidative stress, insulin resistance, inflammation, pancreatic β-cell dysfunction with apoptosis, and eventually diabetic complications, including retinopathy, neuropathy, cardiomyopathy, microvascular complications, and nephropathy [47][48][49][50] .…”

Section: Ages and Diabetesmentioning

confidence: 99%

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

et al. 2021

View full text Add to dashboard Cite

Advanced glycation end products (AGEs) are potentially harmful and heterogeneous molecules derived from nonenzymatic glycation. The pathological implications of AGEs are ascribed to their ability to promote oxidative stress, inflammation, and apoptosis. Recent studies in basic and translational research have revealed the contributing roles of AGEs in the development and progression of various aging-related pathological conditions, such as diabetes, cardiovascular complications, gut microbiome-associated illnesses, liver or neurodegenerative diseases, and cancer. Excessive chronic and/or acute binge consumption of alcohol (ethanol), a widely consumed addictive substance, is known to cause more than 200 diseases, including alcohol use disorder (addiction), alcoholic liver disease, and brain damage. However, despite the considerable amount of research in this area, the underlying molecular mechanisms by which alcohol abuse causes cellular toxicity and organ damage remain to be further characterized. In this review, we first briefly describe the properties of AGEs: their formation, accumulation, and receptor interactions. We then focus on the causative functions of AGEs that impact various aging-related diseases. We also highlight the biological connection of AGE–alcohol–adduct formations to alcohol-mediated tissue injury. Finally, we describe the potential translational research opportunities for treatment of various AGE- and/or alcohol-related adduct-associated disorders according to the mechanistic insights presented.

show abstract

Section: Ages and Diabetesmentioning

confidence: 99%

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Hence, inhibiting RAGE activation may alleviate symptoms of ROS generation, pro-inflammatory cascades, and subsequent endothelial dysfunction. Aminoguanidine, benfotiamine, thiamine, and pyridoxamine have been clinically investigated to treat vascular complications of types 1 and 2 diabetes by inhibition of AGE formation ( 222 ), however the results were mixed. Aminoguanidine showed initial promising results but treatment was later ceased due to adverse events ( 223 ).…”

Section: Therapeutic Strategiesmentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Pre-eclampsia and Gestational Diabetes Mellitus: Windows Into Future Cardiometabolic Health?

et al. 2020

View full text Add to dashboard Cite

Placental insufficiency and adipose tissue dysregulation are postulated to play key roles in the pathophysiology of both pre-eclampsia (PE) and gestational diabetes mellitus (GDM). A dysfunctional release of deleterious signaling motifs can offset an increase in circulating oxidative stressors, pro-inflammatory factors and various cytokines. It has been previously postulated that endothelial dysfunction, instigated by signaling from endocrine organs such as the placenta and adipose tissue, may be a key mediator of the vasculopathy that is evident in both adverse obstetric complications. These signaling pathways also have significant effects on long term maternal cardiometabolic health outcomes, specifically cardiovascular disease, hypertension, and type II diabetes. Recent studies have noted that both PE and GDM are strongly associated with lower maternal flow-mediated dilation, however the exact pathways which link endothelial dysfunction to clinical outcomes in these complications remains in question. The current diagnostic regimen for both PE and GDM lacks specificity and consistency in relation to clinical guidelines. Furthermore, current therapeutic options rely largely on clinical symptom control such as antihypertensives and insulin therapy, rather than that of early intervention or prophylaxis. A better understanding of the pathogenic origin of these obstetric complications will allow for more targeted therapeutic interventions. In this review we will explore the complex signaling relationship between the placenta and adipose tissue in PE and GDM and investigate how these intricate pathways affect maternal endothelial function and, hence, play a role in acute pathophysiology and the development of future chronic maternal health outcomes.

show abstract

“…There is increasing evidence that supports the role of RAGE in the pathogenesis of type 1 diabetes. Hence, blockade of RAGE, its ligands or signal transduction presents a viable target for the secondary prevention of diabetes [58].…”

Section: Plos Onementioning

confidence: 99%

The relationship between advanced glycation end products and gestational diabetes: A systematic review and meta-analysis

et al. 2020

View full text Add to dashboard Cite

Introduction Gestational Diabetes Mellitus (GDM) is a condition in which women without history of diabetes experience hyperglycemia during pregnancy, especially at the second and third trimesters. In women who have had GDM, an elevated body mass index (BMI) may have a substantial impact for persistent hyperglycemia in their lives after gestation. Beyond hyperglycemia, increased local oxidative stress directly promotes the formation of Advanced Glycation End-products (AGEs). Hence, this systematic review and meta-analysis was aimed to determine the relationship between the level of AGEs and/or related metabolic biomarkers with GDM. Methods Literature search was carried out through visiting electronic databases, indexing services, and directories including PubMed/MEDLINE (Ovid ®), EMBASE (Ovid ®), google scholar and WorldCat to retrieve studies without time limit. Following screening and eligibility evaluation, relevant data were extracted from included studies and analyzed using Rev-Man 5.3 and STATA 15.0. Inverse variance method with random effects pooling model was used for the analysis of outcome measures at 95% confidence interval. Hedge's adjusted g statistics was applied to calculate the standardized mean difference (SMD) to consider the small sample bias. Besides, meta-regression, meta-influence, and publication bias analyses were conducted. The protocol has been registered on PROSPERO with ID: CRD42020173867. Results A total of 16 original studies were included for the systematic review and meta-analysis.

show abstract

Targeting the receptor for advanced glycation end products (RAGE) in type 1 diabetes

Cited by 38 publications

References 199 publications

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

Mechanisms of Endothelial Dysfunction in Pre-eclampsia and Gestational Diabetes Mellitus: Windows Into Future Cardiometabolic Health?

The relationship between advanced glycation end products and gestational diabetes: A systematic review and meta-analysis

Contact Info

Product

Resources

About