ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012
Exacerbation of endothelial dysfunction during the progression of diabetes: role of oxidative stress.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Homocysteinylation of Fibrinogen: A Post-Translational Link to Thrombosis.International journal of molecular sciences · 2025Review
- Coronary Microvascular Dysfunction and Heart Failure with Preserved Ejection Fraction - implications for Chronic Inflammatory Mechanisms.Current cardiology reviews · 2022Review
- Circulating metabolites of strawberry mediate reductions in vascular inflammation and endothelial dysfunction in db/db mice.International journal of cardiology · 2018Article
- Role of Adipose Tissue Endothelial ADAM17 in Age-Related Coronary Microvascular Dysfunction.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Divergent outcomes of fructose consumption on exercise capacity of rats: friend or foe.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Biomarkers of Renal Disease and Progression in Patients with Diabetes.Journal of clinical medicine · 2015Review
- Role of homocysteinylation of ACE in endothelial dysfunction of arteries.American journal of physiology. Heart and circulatory physiology · 2015Article
- Effects of 1-Methylnicotinamide (MNA) on Exercise Capacity and Endothelial Response in Diabetic Mice.PloS one · 2015Article
- Preserved Microvascular Endothelial Function in Young, Obese Adults with Functional Loss of Nitric Oxide Signaling.Frontiers in physiology · 2015Article
- Soluble epoxide hydrolase-dependent regulation of myogenic response and blood pressure.American journal of physiology. Heart and circulatory physiology · 2014Article
- Oxidative stress in diabetes: implications for vascular and other complications.International journal of molecular sciences · 2013Review
- COX-2-derived prostanoids and oxidative stress additionally reduce endothelium-mediated relaxation in old type 2 diabetic rats.PloS one · 2013Article
- Altered MAPK signaling in progressive deterioration of endothelial function in diabetic mice.Diabetes · 2012Article
- Hyperglycemia accentuates persistent "functional uncoupling" of cerebral microvascular nitric oxide and superoxide following focal ischemia/reperfusion in rats.Translational stroke research · 2012Article
- CYP2C29 produces superoxide in response to shear stress.Microcirculation (New York, N.Y. : 1994) · 2012Article
- Oxidative stress, Nox isoforms and complications of diabetes--potential targets for novel therapies.Journal of cardiovascular translational research · 2012Review
- Chronic resveratrol treatment protects pancreatic islets against oxidative stress in db/db mice.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
To test the deterioration of endothelial function during the progression of diabetes, shear stress-induced dilation (SSID; 10, 20, and 40 dyn/cm(2)) was determined in isolated mesenteric arteries (80-120 μm in diameter) of 6-wk (6W), 3-mo (3M), and 9-mo (9M)-old male db/db mice and their wild-type (WT) controls. Nitric oxide (NO)-mediated SSID was comparable in 6W WT and db/db mice, but the dilation was significantly reduced in 3M db/db mice and declined further in 9M db/db mice. Vascular superoxide production was progressively increased in 3M and 9M db/db mice, associated with an increased expression of NADPH oxidase. Inhibition of NADPH oxidase significantly improved NO-mediated SSID in arteries of 3M, but not in 9M, db/db mice. Although endothelial nitric oxide synthase (eNOS) expression was comparable in all groups, a progressive reduction in shear stress-induced eNOS phosphorylation existed in vessels of 3M and 9M db/db mice. Moreover, inducible NOS (iNOS) that was not detected in WT, nor in 6W and 3M db/db mice, was expressed in vessels of 9M db/db mice. A significantly increased expression of nitrotyrosine in total protein and immunoprecipitated eNOS was also found in vessels of 9M db/db mice. Thus, impaired NO bioavailability plays an essential role in the endothelial dysfunction of diabetic mice, which becomes aggravated when endothelial nitrosative stress is further activated via perhaps, an additional iNOS-mediated pathway during the progression of diabetes.
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Registered trials
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