Endothelial MnSOD overexpression prevents retinal VEGF expression in diabetic mice

Goto, Hideo; Nishikawa, Takeshi; Sonoda, Kazuhiro; Kondo, Tatsuya; Kukidome, Daisuke; Fujisawa, Kazuo; Yamashiro, Tsuyoshi; Motoshima, Hiroyuki; Matsumura, Takeshi; Tsuruzoe, Kaku; Araki, Eiichi

doi:10.1016/j.bbrc.2007.12.041

Cited by 39 publications

(24 citation statements)

References 31 publications

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“…Probably, it prevents the development of diabetic retinopathy in vivo. 41 Similar results were obtained in the study of Kowluru et al, 42 in which the overexpression of MnSOD in diabetes--induced mice maintained a physiological level of glutathione,8 -hydroxy -2'-deoxyguanosine, and nitrotyrosine, which may inhibit the development of retinopathy.…”

Section: -42supporting

confidence: 78%

Expression of mitochondrial superoxide dismutase in polymorphonuclear leukocytes from patients with type 1 diabetes with and without microvascular complications

Wegner

Rawłuszko-Wieczorek²,

Araszkiewicz³

et al. 2014

Polish Archives of Internal Medicine

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Section: -42supporting

confidence: 78%

Expression of mitochondrial superoxide dismutase in polymorphonuclear leukocytes from patients with type 1 diabetes with and without microvascular complications

Wegner

Rawłuszko-Wieczorek²,

Araszkiewicz³

et al. 2014

Polish Archives of Internal Medicine

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“…Mitochondrial-derived oxidative stress has also been implicated in chronic inflammation, cancer progression (206), diabetes mellitus (148,152,(317)(318)(319)378), and atherosclerosis (21,258). Mitochondrial-derived ROS (MtROS) also contributes to LPS-mediated production of pro-inflammatory cytokines IL-1b, IL-6, and TNF-a (48).…”

Section: B Mitochondrial-derived Ros In Inflammationmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,516

2,424

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Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

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“…One possible way to reduce ROI is the detoxification of superoxide radicals by increasing superoxide dismutase (SOD). A recent study in mice with overexpression of SOD in their endothelial cells has shown that the progression of diabetic retinopathy in vivo can be suppressed by reducing the expression of VEGF and fibronectin (Goto et al 2008). Other ways of scavenging ROI or of inhibiting ROI generating NADPH oxidase in vascular cells are presently being evaluated.…”

Section: Hyperglycemiamentioning

confidence: 99%

Endothelial dysfunction and diabetes: roles of hyperglycemia, impaired insulin signaling and obesity

et al. 2008

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Endothelial dysfunction comprises a number of functional alterations in the vascular endothelium that are associated with diabetes and cardiovascular disease, including changes in vasoregulation, enhanced generation of reactive oxygen intermediates, inflammatory activation, and altered barrier function. Hyperglycemia is a characteristic feature of type 1 and type 2 diabetes and plays a pivotal role in diabetesassociated microvascular complications. Although hyperglycemia also contributes to the occurrence and progression of macrovascular disease (the major cause of death in type 2 diabetes), other factors such as dyslipidemia, hyperinsulinemia, and adipose-tissue-derived factors play a more dominant role. A mutual interaction between these factors and endothelial dysfunction occurs during the progression of the disease. We pay special attention to the possible involvement of endoplasmic reticulum stress (ER stress) and the role of obesity and adipose-derived adipokines as contributors to endothelial dysfunction in type 2 diabetes. The close interaction of adipocytes of perivascular adipose tissue with arteries and arterioles facilitates the exposure of their endothelial cells to adipokines, particularly if inflammation activates the adipose tissue, and thus affects vasoregulation and capillary recruitment in skeletal muscle. Hence, an initial dysfunction of endothelial cells underlies metabolic and vascular alterations that contribute to the development of type 2 diabetes.

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Endothelial MnSOD overexpression prevents retinal VEGF expression in diabetic mice

Cited by 39 publications

References 31 publications

Expression of mitochondrial superoxide dismutase in polymorphonuclear leukocytes from patients with type 1 diabetes with and without microvascular complications

Expression of mitochondrial superoxide dismutase in polymorphonuclear leukocytes from patients with type 1 diabetes with and without microvascular complications

Reactive Oxygen Species in Inflammation and Tissue Injury

Endothelial dysfunction and diabetes: roles of hyperglycemia, impaired insulin signaling and obesity

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