Overexpression of mitochondrial superoxide dismutase in mice protects the retina from diabetes-induced oxidative stress

Kowluru, Renu A.; Kowluru, Vibhuti; Xiong, Ye; Ho, Ye Shih

doi:10.1016/j.freeradbiomed.2006.01.012

Cited by 203 publications

(180 citation statements)

References 38 publications

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“…In particular, exogenous antioxidants [12,13] or overproduction of endogenous defence enzymes such as mitochondrial SOD protect against the development of retinal microvascular lesions in animal models of diabetes [14,15]. Despite this, results from clinical studies have failed to unambiguously establish if oxidative stress plays any role in the development of retinopathy in diabetic patients.…”

Section: Discussionmentioning

confidence: 99%

“…Investigation of appropriate animal models strongly supports the premise that oxidative stress plays an important role in the pathogenesis of diabetic retinopathy. Superoxide levels are elevated in the diabetic retina [10,11] and inhibition of superoxide accumulation with antioxidants [12,13] or overproduction of mitochondrial superoxide dismutase (SOD) [14,15] can prevent lesions of retinopathy in experimentally induced diabetes in rodents.…”

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confidence: 99%

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Evaluation of N ε-(3-formyl-3,4-dehydropiperidino)lysine as a novel biomarker for the severity of diabetic retinopathy

et al. 2008

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Aims/hypothesis Recent studies suggest that oxidative stress should be monitored alongside HbA 1c to identify subgroups of diabetic patients at high risk of initiation or progression of retinopathy. The acrolein-derived advanced lipoxidation end-product (ALE), N " -(3-formyl-3,4-dehydropiperidino)lysine (FDP-lysine), is a useful biomarker that reflects the cumulative burden of oxidative stress over long periods of time. The purpose of the present study was to investigate whether serum and haemoglobin levels of FDP-lysine are associated with the severity of diabetic retinopathy in type 1 and type 2 diabetic patients. Methods Serum and haemoglobin levels of FDP-lysine were measured by competitive ELISA in 59 type 1 and 76 type 2 diabetic patients with no retinopathy, non-proliferative retinopathy or proliferative retinopathy (mean age [±SEM] 54.3±1.3 years), and in 47 non-diabetic control individuals (mean age 51.9±2.1 years).Results Serum and haemoglobin levels of FDP-lysine were significantly increased in diabetic patients compared with control individuals (p=0.04 and p=0.002, respectively). However, no significant association was found between levels of serum FDP-lysine and the severity of diabetic retinopathy (p=0.97). In contrast, increased haemoglobin FDP-lysine levels were observed in patients with proliferative retinopathy compared with patients without retinopathy and with non-proliferative retinopathy (p=0.04). The relationship of FDP-lysine with proliferative retinopathy was unaltered after adjustment for HbA 1c , or other clinical parameters. Conclusions/interpretation Our data suggest that haemoglobin FDP-lysine may provide a useful risk marker for the development of proliferative diabetic retinopathy independently of HbA 1c , and that elevated intracellular ALE formation may be involved in the pathogenesis of this sight-threatening complication of diabetes.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Evaluation of N ε-(3-formyl-3,4-dehydropiperidino)lysine as a novel biomarker for the severity of diabetic retinopathy

et al. 2008

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“…It has been reported that overproduction of mitochondrial superoxide dismutase (SOD) [36] and inhibition of superoxide with antioxidants [37,38] can protect against capillary degeneration during diabetic retinopathy in experimental diabetes, although how this influences AGE accumulation in the retina has not been studied. It is also possible that some chelators may shift the redox potential of iron or copper, affecting their catalytic activity in a way that could exacerbate oxidative stress and diabetes complications.…”

Section: Accumulation Of Agesmentioning

confidence: 99%

“…Increasing evidence suggests that AGE receptor binding can initiate important signaling pathways involving tyrosine phosphorylation of Janus kinase (JAK)/signal transducers and activators of transcription (STAT) [36], recruitment of phosphatidylinositol 3 kinase to Ras [37], activation of protein kinase C [38], and oxidative stress through NFkB and AP-1 transcription [39]. AGEs interact with cells through several routes.…”

Section: Accumulation Of Agesmentioning

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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“…1,2 Oxidative stress plays a major role in the pathogenesis of atherosclerosis, diabetic nephropathy and diabetic retinopathy within the chronic kidney disease population. [3][4][5][6] In addition, oxidative stress is an important determinant of acute kidney failure. 7,8 In some studies, ROS has been advanced as a factor in the pathogenesis of both ischemic and nephrotoxic kidney damage.…”

Section: Introductionmentioning

confidence: 99%

Manganese superoxide dismutase, glutathione peroxidase and catalase gene polymorphisms and clinical outcomes in acute kidney injury

Kıdır

Yiğit

et al. 2016

Renal Failure

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Introduction The aim of this study was to evaluate the potential association of single gene polymorphisms of manganese superoxide dismutase (MnSOD), glutathione peroxidase 1 (GPX1) and catalase (CAT) with clinical outcomes of acute kidney injury (AKI). Materials and methods Ninety AKI patients and 101 healthy volunteers were included in the study. Determination of MnSOD rs4880, GPX1 rs1050450 and CAT rs769217 polymorphisms was performed using real-time polymerase chain reaction amplification. The duration of hospitalization of AKI patients, dialysis and intensive care requirements, sepsis, oliguria and in-hospital mortality rates were assessed. Results The MnSOD, GPX1 and CAT genotypes and allele frequencies of AKI patients did not differ significantly from those of healthy controls. In patients with a T allele in the ninth exon of the CAT gene, intensive care requirements were greater than those of patients with the CC genotype (p ¼ 0.04). In addition, sepsis and in-hospital mortality were observed significantly more frequently in patients with a T allele in the ninth exon of the CAT gene (p ¼ 0.03). Logistic regression analysis determined that bearing a T allele was the primary determinant of intensive care requirements and in-hospital mortality, independent of patient age, gender, presence of diabetes and dialysis requirements (OR 6.10, 95% CI 1.34-27.81, p ¼ 0.02 and OR 10.25, 95% CI 1.13-92.80, p ¼ 0.04, respectively). Conclusion Among AKI patients in the Turkish population, hospital morbidity and mortality were found to be more frequent in patients bearing a T allele of the rs769217 polymorphism of the CAT gene.

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Overexpression of mitochondrial superoxide dismutase in mice protects the retina from diabetes-induced oxidative stress

Cited by 203 publications

References 38 publications

Evaluation of N ε-(3-formyl-3,4-dehydropiperidino)lysine as a novel biomarker for the severity of diabetic retinopathy

Evaluation of N ε-(3-formyl-3,4-dehydropiperidino)lysine as a novel biomarker for the severity of diabetic retinopathy

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

Manganese superoxide dismutase, glutathione peroxidase and catalase gene polymorphisms and clinical outcomes in acute kidney injury

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