ArticlePloS one2013
Akita spontaneously type 1 diabetic mice exhibit elevated vascular arginase and impaired vascular endothelial and nitrergic function.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Novel Role of AcylCoA: Cholesterol Acyltransferase 1/Sterol O-Acyltransferase 1 (ACAT1/SOAT1) in Diabetic Retinopathy.Investigative ophthalmology & visual science · 2026Article
- Erectile Dysfunction in Diabetes Mellitus: A Comprehensive Narrative Review of Pathophysiology, Genetic Association Studies and Therapeutic Approaches.Endocrinology, diabetes & metabolism · 2025Review
- Inhibition of neutrophil extracellular trap formation alleviates vascular dysfunction in type 1 diabetic mice.Science advances · 2023Article
- Coronary Microvascular Dysfunction in Diabetes Mellitus: Pathogenetic Mechanisms and Potential Therapeutic Options.Biomedicines · 2022Review
- Interleukin-35 Prevents the Elevation of the M1/M2 Ratio of Macrophages in Experimental Type 1 Diabetes.International journal of molecular sciences · 2022Article
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice.Frontiers in cardiovascular medicine · 2022Article
- Arginase: Biological and Therapeutic Implications in Diabetes Mellitus and Its Complications.Oxidative medicine and cellular longevity · 2022Review
- Hypoxia Induces Renal Epithelial Injury and Activates Fibrotic Signaling Through Up-Regulation of Arginase-II.Frontiers in physiology · 2021Article
- Protein kinase A facilitates relaxation of mouse ileum via phosphorylation of neuronal nitric oxide synthase.British journal of pharmacology · 2020Article
- Article
- Deletion of endothelial arginase 1 does not improve vasomotor function in diabetic mice.Physiological reports · 2018Article
- Mechanisms of Diabetes-Induced Endothelial Cell Senescence: Role of Arginase 1.International journal of molecular sciences · 2018Article
- Evaluation of Notch3 Deficiency in Diabetes-Induced Pericyte Loss in the Retina.Journal of vascular research · 2018Article
- Obesity-induced vascular dysfunction and arterial stiffening requires endothelial cell arginase 1.Cardiovascular research · 2017Article
- Coronary microvascular disease as an early culprit in the pathophysiology of diabetes and metabolic syndrome.Pharmacological research · 2017Review
- The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activator dh404 protects against diabetes-induced endothelial dysfunction.Cardiovascular diabetology · 2017Article
- A novel experimental model of erectile dysfunction in rats with heart failure using volume overload.PloS one · 2017Article
- Article
- Targeted overexpression of endothelial nitric oxide synthase in endothelial cells improves cerebrovascular reactivity in Ins2Akita-type-1 diabetic mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Deregulation of arginase induces bone complications in high-fat/high-sucrose diet diabetic mouse model.Molecular and cellular endocrinology · 2016Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundElevated arginase (Arg) activity is reported to be involved in diabetes-induced vascular endothelial dysfunction. It can reduce L-arginine availability to nitric oxide (NO) synthase (NOS) and NO production. Akita mice, a genetic non-obese type 1 diabetes model, recapitulate human diabetes. We determined the role of Arg in a time-course of diabetes-associated endothelial dysfunction in aorta and corpora cavernosa (CC) from Akita mice. METHODS AND
resultsEndothelium-dependent relaxation, Arg and NOS activity, and protein expression levels of Arg and constitutive NOS were assessed in aortas and CC from Akita and non-diabetic wild type (WT) mice at 4, 12 and 24 wks of age. Systolic blood pressure (SBP) was assessed by tail cuff. In aorta and CC, Akita mice exhibited a progressive impairment of vascular endothelial and nitrergic function increased Arg activity and expression (Arg1 in aorta and both Arg1 and Arg2 in CC) compared with that of age-matched WT mice. Treatment of aorta and CC from Akita mice with an Arg inhibitor (BEC or ABH) reduced diabetes-induced elevation of Arg activity and restored endothelial and nitrergic function. Reduced levels of phospho-eNOS at Ser(1177) (in aorta and CC) and nNOS expression (in CC) were observed in Akita mice at 12 and 24 wks. Akita mice also had decreased NOS activity in aorta and CC at 12 and 24 wks that was restored by BEC treatment. Further, Akita mice exhibited moderately increased SBP at 24 wks and increased sensitivity to PE-induced contractions in aorta and sympathetic nerve stimulation in CC at 12 and 24 wks.
conclusionsOver 24 wks of diabetes in Akita mice, both aortic and cavernosal tissues exhibited increased Arg activity/expression, contributing to impaired endothelial and nitrergic function and reduced NO production. Our findings demonstrate involvement of Arg activity in diabetes-induced impairment of vascular function in Akita mouse.
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