2000
DOI: 10.1038/35008121
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Abstract: Diabetic hyperglycaemia causes a variety of pathological changes in small vessels, arteries and peripheral nerves. Vascular endothelial cells are an important target of hyperglycaemic damage, but the mechanisms underlying this damage are not fully understood. Three seemingly independent biochemical pathways are involved in the pathogenesis: glucose-induced activation of protein kinase C isoforms; increased formation of glucose-derived advanced glycation end-products; and increased glucose flux through the aldo… Show more

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Cited by 3,837 publications
(3,023 citation statements)
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References 24 publications
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“…This leads to enhanced mitochondrial O 2 − generation, mainly due to auto-oxidation of ubiquinol [157][158][159]. Thus, it can be argued that the mitochondria can transduce a nitrosative signal into an oxidative signal, consistent with the proposed role of mitochondrial ROS in cytosolic signaling pathways [143].…”
Section: Apoptosis Mitochondrial Function and Mapk Signal Transductionsupporting
confidence: 53%
See 1 more Smart Citation
“…This leads to enhanced mitochondrial O 2 − generation, mainly due to auto-oxidation of ubiquinol [157][158][159]. Thus, it can be argued that the mitochondria can transduce a nitrosative signal into an oxidative signal, consistent with the proposed role of mitochondrial ROS in cytosolic signaling pathways [143].…”
Section: Apoptosis Mitochondrial Function and Mapk Signal Transductionsupporting
confidence: 53%
“…In fact, the burst of mitochondrial O 2 − generation associated with apoptosis has been linked to cytochrome c release from mitochondria, and can be prevented by Bcl-2 over-expression [26]. The vectorial release of mitochondrial O 2 − (more correctly, H 2 O 2 ) to the cytosol may, in turn, be important in cell signaling [143], e.g. activation of MAPK such as JNK [135,218].…”
Section: Apoptosis Mitochondrial Function and Mapk Signal Transductionmentioning
confidence: 99%
“…Increases in reactive oxygen species are prevented by SOD2 [28]. Impaired expression of SOD2 or other genes associated with a stress defence system, including FMO5, as observed here and in ob/ob mice [11], could increase oxidative stress in the diabetic state.…”
Section: Discussionmentioning
confidence: 52%
“…Hyperglycaemia increases the production of reactive oxygen species, which may activate protein kinase C, induces advanced glycation end-product formation and activates the pleiotropic transcription factor, nuclear factor-kappa B [28]. Increases in reactive oxygen species are prevented by SOD2 [28].…”
Section: Discussionmentioning
confidence: 99%
“…Using clonal beta cells, others show that UCP2 overexpression reduces cell death induced by application of H 2 O 2 [129]. Increased uncoupling in vascular endothelial cells induced by UCP1 overexpression reduces ROS formation caused by hyperglycaemia [130]. Since UCP1 is not likely to be expressed naturally in endothelia, UCP2 could be a candidate for such function under physiological conditions.…”
Section: Regulation Of Reactive Oxygen Species Productionmentioning
confidence: 99%