The pathobiology of diabetic complications: a unifying mechanism.
By M. Brownlee. Diabetes, 2005
5,502 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Surgery
View Paper: https://www.semanticscholar.org/paper/68625af9171636fbefcedfac74f06bb1789eaf98
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
- P. Chan
- L. Cañedo-Dorantes
- Mara Cañedo-Ayala
- A. Lo
- Andrzej Grzybowski
- Qingzheng Kang
- J. L. Edwards
- Eva L. Feldman
In Genetics
- P. Chan
- L. Cañedo-Dorantes
- Mara Cañedo-Ayala
- A. Lo
- Andrzej Grzybowski
- Qingzheng Kang
- J. L. Edwards
- Eva L. Feldman
In Surgery
- P. Chan
- L. Cañedo-Dorantes
- Mara Cañedo-Ayala
- A. Lo
- Andrzej Grzybowski
- Qingzheng Kang
- J. L. Edwards
- Eva L. Feldman
Citations in the corpus
- Periodontitis and diabetes: a two-way relationship (2011, background): “The elevated inflammatory state in diabetes contributes to both microvascular and macrovascular complications, and it is clear that hyperglycaemia can result in the activation of pathways that increase inflammation, oxidative stress and apoptosis [41].”
- Reactive Oxygen Species (2014, background): “For example, in diabetes hyperglycemia causes leakage of electrons from mitochondrial electron transport chain which results in the increased reduction of molecular oxygen and production of superoxide [1].”
- Oxidative Stress and Diabetic Retinopathy (2007, background): “Hyperglycemia-induced overproduction of superoxide by the mitochondrial electron transport chain is considered to activate the major pathways of hyperglycemic damage by inhibiting GAPDH activity, and glucose-induced increase in superoxide induces mutations in mitochondrial DNA resulting in defective”
- Vascular endothelial growth factor in eye disease. (2008, background): “All of these events have been suggested to be initiated by superoxide overproduction by the mitochondrial electron-transport chain (Brownlee, 2005).”
- Molecular mechanisms of diabetic kidney disease. (2014, neutral): “Increased reactive oxygen species (ROS) and superoxide generation by dysfunctional mitochondria in diabetes has been postulated as the primary initiating event in the development of diabetic complications (37, 38).”
- Cardiovascular actions of insulin. (2007, background): “ROS also activates PKC- , PKC- , and PKC- , leading to decreased expression of eNOS and increased expression of ET-1, VEGF, and TGFin endothelial cells (237).”
- Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms (2017, background): “Chronic hyperglycemia and insulin resistance play an important role in the initiation of vascular complications of diabetes and involve a number of mechanisms including (1) increased formation of advanced glycation end products (AGEs) and activation of the receptor for advanced glycation end product”
- Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “The damage inflicted by ROS has been implicated in conditions of inflammation, diabetes mellitus, age-related degeneration and tumour formation (Evans et al. 2002; Brownlee, 2005; Greenman et al. 2007).”
- Role of ROS and RNS Sources in Physiological and Pathological Conditions (2016, background): “In this context, the presence of mitochondrial impairment has been demonstrated in different types of leukocytes [359] and tissues such as liver, lung, skeletal muscle, spleen, or heart in type 2 diabetes [360, 361], confirming the relationship between this condition and mitochondrial dysfunction.”