Clinical implications of oxidative stress and potential role of natural antioxidants in diabetic vascular complications

Ceriello, Antonio; Testa, Roberto; Genovese, Stefano

doi:10.1016/j.numecd.2016.01.006

Cited by 96 publications

(61 citation statements)

References 115 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Despite prominent advances in diabetes treatment, glucose monitoring and biomarkers of glycaemic control, detrimental vascular complications still remain in most diabetic patients [2]. Diabetes is associated with significantly accelerated rates of several macrovascular complications such as atherosclerosis, diabetic cardiomyopathy (DCM) and other cardiovascular diseases and microvascular complications such as nephropathy and retinopathy [3,4]. Diabetic cardiovascular diseases are the main cause of disability and death of diabetic patients [5].…”

Section: Introductionmentioning

confidence: 99%

Novel insights into DNA methylation and its critical implications in diabetic vascular complications

et al. 2017

View full text Add to dashboard Cite

Recent epidemiological and clinical studies have shown that type 2 diabetic patients can develop diabetic vascular complications even after intensive glycaemic control. It has been suggested that this phenomenon could be explained by the hypothesis of ‘metabolic memory’. The underlying mechanisms between these enduring effects and the prior hyperglycaemic state are still not well understood. Preliminary studies demonstrate that hyperglycaemia can regulate gene expression by epigenetic modifications, such as DNA methylation, which can persistently exist even after glucose normalization. Increasing evidence shows that epigenetic mechanisms may play a substantial role in the pathophysiology of diabetes and its associated vascular complications, including atherosclerosis, diabetic cardiomyopathy (DCM), nephropathy and retinopathy. In this review, we will examine the growing role of DNA methylation in diabetes and its vascular complications, thus it can provide critical implications for the early prevention of diabetes and its vascular complications.

show abstract

Section: Introductionmentioning

confidence: 99%

Novel insights into DNA methylation and its critical implications in diabetic vascular complications

et al. 2017

View full text Add to dashboard Cite

show abstract

“…It is defined traditionally by kidney morphological and functional modifications like; glomerular hyperfiltration, glomerular and kidney hypertrophy, increased urinary albumin excretion, increased glomerular basement membrane (GBM) thickness, and mesangial expansion and also accumulation of extracellular proteins comprising laminin, collagens and fibronectin (17,18). It is now clear that multiple pathways are involved in the pathogenesis of diabetic kidney disease like; hexosamine pathway, protein kinase C (PKC) pathway, formation of advanced glycation end products (AGEs), polyol pathway, growth factors, cytokines and free radicals.…”

Section: Oxidative Stress and Diabetic Nephropathymentioning

confidence: 99%

“…Also, the evidence show that oxidative stress during diabetic kidney disease eventually results to the knocking down of normal kidney homeostasis and its proper functioning. It is well established that augmented ROS construction in kidneys of both type 1 and type 2 DM can be affected individuals through both enzymatic and non-enzymatic pathways (18). …”

Section: Oxidative Stress and Diabetic Nephropathymentioning

confidence: 99%

An update on diabetic kidney disease, oxidative stress and antioxidant agents

et al. 2017

View full text Add to dashboard Cite

Diabetes mellitus is a metabolic disease that is defined by relative or absolute deficiency of insulin secretion. Diabetic kidney disease seems to be one of the most frequent complications of diabetes mellitus. Based on evidence, increased free-radical formation and/or diminished antioxidant defenses induce oxidative stress that is implicated in the pathogenesis of diabetic kidney disease. It is evident that diabetic state induces oxidative stress through different signaling pathways as well as reactive oxygen species (ROS) formation that attributes to the activation of various downstream signaling cascade leading to structural the way to structural and functional changes in kidney.

show abstract

“…Anti-oxidant molecules may protect from endothelial dysfunction by re-coupling eNOS activity, reduce superoxide production, increase the activity of superoxide scavenging enzymes, or decrease vascular NAD(P)H oxidase activity [251,252]. Novel antioxidant therapies aiming to restore production of endothelialderived NO or to act as endogenous antioxidant enzymes may represent a more targeted strategy focusing specifically on the mechanisms implicated in diabetes-induced endothelial dysfunction (reviewed in [240].…”

Section: Rock (Rho-associated Kinase) Inhibitors -mentioning

confidence: 99%

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Potenza

Nacci

Salvia

et al. 2017

Pharmacological Research

View full text Add to dashboard Cite

Abstract:The association of obesity and diabetes, termed "diabesity", defines a combination of primarily metabolic disorders with insulin resistance as the underlying common pathophysiology. Cardiovascular disorders associated with diabesity represent the leading cause of morbidity and mortality in the Western world. This makes diabesity, with its rising impacts on both health and economics, one of the most challenging biomedical and social threats of present century. The emerging comprehension of the genes whose alteration confers inter-individual differences on risk factors for diabetes or obesity, together with the potential role of genetically determined variants on mechanisms controlling responsiveness, effectiveness and safety of anti-diabetic therapy underlines the need of additional knowledge on molecular mechanisms involved in the pathophysiology of diabesity. Endothelial cell dysfunction, resulting from the unbalanced production of endothelialderived vascular mediators, is known to be present at the earliest stages of insulin resistance and obesity, and may precede the clinical diagnosis of diabetes by several years. Once considered as a mere consequence of metabolic abnormalities, it is now clear that endothelial dysfunctional activity may play a pivotal role in the progression of diabesity. In the vicious circle where vascular defects and metabolic disturbances worsen and reinforce each other, a low-grade, chronic, and 'cold' inflammation (metaflammation) has been suggested to serve as the pathophysiological link that binds endothelial and metabolic dysfunctions. In this paradigm, it is important to consider how traditional antidiabetic treatments (specifically addressing metabolic dysregulation) may directly impact on inflammatory processes or cardiovascular function. Indeed, not all drugs currently available to treat diabetes possess the same anti-inflammatory potential, or target endothelial cell function equally. Perspective strategies pointing at reducing metaflammation or directly addressing endothelial dysfunction may disclose beneficial consequences on metabolic regulation. This review focuses on existing and potential new approaches ameliorating endothelial dysfunction and vascular inflammation in the context of diabesity.

show abstract

Clinical implications of oxidative stress and potential role of natural antioxidants in diabetic vascular complications

Cited by 96 publications

References 115 publications

Novel insights into DNA methylation and its critical implications in diabetic vascular complications

Novel insights into DNA methylation and its critical implications in diabetic vascular complications

An update on diabetic kidney disease, oxidative stress and antioxidant agents

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Contact Info

Product

Resources

About