Oxidative Retinal Products and Ocular Damages in Diabetic Patients

Grattagliano, Ignazio; Vendemiale, Gianluigi; Boscia, Francesco; Micelli-Ferrari, T; Cardia, Luigi; Altomare, Emanuele

doi:10.1016/s0891-5849(98)00059-8

Cited by 79 publications

(54 citation statements)

References 28 publications

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“…In fact, oxidative stress plays an important role in the pathogenesis of vascular alterations by either triggering or exacerbating the biochemical processes accompanying the metabolic syndrome [48]. In addition, experimental and clinical observations indicate oxidative stress as an important mechanism in obesity-associated metabolic syndrome, in the development of diabetes and its complications and in "satellite" conditions such as nonalcoholic steatohepatitis (NASH) [49][50][51][52].…”

Section: Oxidative Stress and Metabolic Syndromementioning

confidence: 99%

Metabolic Syndrome, Aging and Involvement of Oxidative Stress

Bonomini¹,

Rodella²,

Rezzani³

2015

Aging and disease

467

308

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ABSTRACT:The prevalence of the metabolic syndrome, a cluster of cardiovascular risk factors associated with obesity and insulin resistance, is dramatically increasing in Western and developing countries. This disorder consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart diseases. One of the defects in metabolic syndrome and its associated diseases is excess of reactive oxygen species. Reactive oxygen species generated by mitochondria, or from other sites within or outside the cell, cause damage to mitochondrial components and initiate degradative processes. Such toxic reactions contribute significantly to the aging process. In this article we review current understandings of oxidative stress in metabolic syndrome related disease and its possible contribution to accelerated senescence.

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Section: Oxidative Stress and Metabolic Syndromementioning

confidence: 99%

Metabolic Syndrome, Aging and Involvement of Oxidative Stress

Bonomini¹,

Rodella²,

Rezzani³

2015

Aging and disease

467

308

View full text Add to dashboard Cite

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“…In diabetic animals, AGE inhibitors such as aminoguanidine can attenuate the formation of retinal microvascular lesion; however, recent studies indicate that this drug can significantly alleviate diabetic retinopathic lesions without affecting the formation of the AGE pentosidine in retinal basement membrane collagen [89]. This effect might be linked with aminoguanidine's antioxidative property rather than AGE inhibitory properties [90] as oxidative imbalances in diabetic retinopathy have also been extensively reported [91,92]. Interestingly, some studies have reported no significant change of retinal vascular lesions after treatment with antioxidants [93].…”

Section: Age Inhibitors and Prevention Of Retinopathymentioning

confidence: 99%

Molecular mechanisms of Diabetic Retinopathy, general preventive strategies and novel therapeutic targets

Safi¹,

Qvist²,

Kumar³

et al. 2013

Exp Clin Endocrinol Diabetes

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The growing number of people with diabetes worldwide suggests that diabetic retinopathy (DR) and diabetic macular edema (DME) will continue to be sight threatening factors. The pathogenesis of diabetic retinopathy is a widespread cause of visual impairment in the world and a range of hyperglycemia-linked pathways have been implicated in the initiation and progression of this condition. Despite understanding the polyol pathway flux, activation of protein kinase C (KPC) isoforms, increased hexosamine pathway flux, and increased advanced glycation end-product (AGE) formation, pathogenic mechanisms underlying diabetes induced vision loss are not fully understood. The purpose of this paper is to review molecular mechanisms that regulate cell survival and apoptosis of retinal cells and discuss new and exciting therapeutic targets with comparison to the old and inefficient preventive strategies. This review highlights the recent advancements in understanding hyperglycemia-induced biochemical and molecular alterations, systemic metabolic factors, and aberrant activation of signaling cascades that ultimately lead to activation of a number of transcription factors causing functional and structural damage to retinal cells. It also reviews the established interventions and emerging molecular targets to avert diabetic retinopathy and its associated risk factors.

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“…While intimately linked with AGE formation, oxidative imbalances in diabetic retinopathy have also been widely reported (23)(24)(25)(26). Vitamin E (VE) can cause normalization of diabetes-related retinal blood flow abnormalities (27), while this antioxidant, in combination with vitamin C, can inhibit capillary cell death (28).…”

mentioning

confidence: 99%

The AGE Inhibitor Pyridoxamine Inhibits Development of Retinopathy in Experimental Diabetes

et al. 2002

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We examined the ability of pyridoxamine (PM), an inhibitor of formation of advanced glycation end products (AGEs) and lipoxidation end products (ALEs), to protect against diabetes-induced retinal vascular lesions. The effects of PM were compared with the antioxidants vitamin E (VE) and R-␣-lipoic acid (LA) in streptozotocin-induced diabetic rats. Animals were given either PM (1 g/l drinking water), VE (2,000 IU/kg diet), or LA (0.05%/kg diet). After 29 weeks of diabetes, retinas were examined for pathogenic changes, alterations in extracellular matrix (ECM) gene expression, and accumulation of the immunoreactive AGE/ALE N -(carboxymethyl)lysine (CML). Acellular capillaries were increased more than threefold, accompanied by significant upregulation of laminin immunoreactivity in the retinal microvasculature. Diabetes also increased mRNA expression for fibronectin (2-fold), collagen IV (1.6-fold), and laminin ␤ chain (2.6-fold) in untreated diabetic rats compared with nondiabetic rats. PM treatment protected against capillary drop-out and limited laminin protein upregulation and ECM mRNA expression and the increase in CML in the retinal vasculature. VE and LA failed to protect against retinal capillary closure and had inconsistent effects on diabetes-related upregulation of ECM mRNAs. These results indicate that the AGE/ALE inhibitor PM protected against a range of pathological changes in the diabetic retina and may be useful for treating diabetic retinopathy.

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Oxidative Retinal Products and Ocular Damages in Diabetic Patients

Cited by 79 publications

References 28 publications

Metabolic Syndrome, Aging and Involvement of Oxidative Stress

Metabolic Syndrome, Aging and Involvement of Oxidative Stress

Molecular mechanisms of Diabetic Retinopathy, general preventive strategies and novel therapeutic targets

The AGE Inhibitor Pyridoxamine Inhibits Development of Retinopathy in Experimental Diabetes

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