Oxidative Stress as a Major Culprit in Kidney Disease in Diabetes
By J. Forbes, M. Coughlan, M. Cooper. Diabetes, 2008
1,212 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Nephrology
View Paper: https://www.semanticscholar.org/paper/bbd38b68d3171a0fbe7f5c738a3580f1bf2052ee
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In Clinical Biochemistry
In Nephrology
Citations in the corpus
- Oxidant Mechanisms in Renal Injury and Disease (2016, positive): “…factor involved in initiation and progression of various mammalian kidney diseases and injuries, including diabetic nephropathy, hypertension-related kidney injury, ischemia–reperfusion injury (IRI), toxic-induced nephropathy, and several forms of inflammatory syndromes (29, 75, 148, 278, 297).”
- Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment (2021, background): “On the other hand, as in the previous explanation, the increase in ROS due to hyperglycemia is central to the pathogenesis of DN [22, 29], and ROS plays an important role in the induction and progression of DN [29, 76].”
- Oxidative stress: an essential factor in the pathogenesis of gastrointestinal mucosal diseases. (2014, background): “Oxidative and nitrosative stress have been etiologically implicated in a wide variety of disease processes and states: aging, I/R injury, hypertension, atherosclerosis, diabetic neuropathies, renal diseases, neurological diseases including Alzheimer’s disease and other forms of dementia, as well as ”
- Relationship between oxidative stress and inflammatory cytokines in diabetic nephropathy. (2012, background): “Recent evidence suggests that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the primary source of vascular and renal ROS production [30–36]; however, other possible sources include glucose-6-phosphate dehydrogenase, flux through the sorbitol/polyol pathway, and glycation of free ami”