ArticleEndocrinology2012
Angiotensin-(1-7) administration reduces oxidative stress in diabetic bone marrow.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- Angiotensin (1-7) exaggerates albuminuria and nephrin gene expression but does not modulate renal function-specific microRNAs expressions in kidneys of db/db mice.Acta diabetologica · 2026Article
- The potential role of nitrate, a nitric oxide donor, in the prevention and treatment of diabetic osteoporosis.Frontiers in endocrinology · 2025Review
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- Angiotensin-(1-7) attenuates collagen-induced arthritis via inhibiting oxidative stress in rats.Amino acids · 2021Article
- Diabetoporosis: Role of nitric oxide.EXCLI journal · 2021Review
- COVID-19 and Hypertension: The What, the Why, and the How.Frontiers in physiology · 2021Review
- Targeting Angiotensin-Converting Enzyme-2/Angiotensin-(1-7)/Mas Receptor Axis in the Vascular Progenitor Cells for Cardiovascular Diseases.Molecular pharmacology · 2021Review
- Involvement of dopaminergic signaling in the cross talk between the renin-angiotensin system and inflammation.Seminars in immunopathology · 2020Review
- Angiotensin-(1-7) Expressed From Lactobacillus Bacteria Protect Diabetic Retina in Mice.Translational vision science & technology · 2020Article
- Targeting the Protective Arm of the Renin-Angiotensin System to Reduce Systemic Lupus Erythematosus Related Pathologies in MRLFrontiers in immunology · 2020Article
- Improving the Innate Immune Response in Diabetes by Modifying the Renin Angiotensin System.Frontiers in immunology · 2019Article
- Long-Term Administration of Angiotensin (1-7) toOxidative medicine and cellular longevity · 2018Article
- Reversal of Bone Marrow Mobilopathy and Enhanced Vascular Repair by Angiotensin-(1-7) in Diabetes.Diabetes · 2017Article
- Long-term administration of angiotensin (1-7) prevents heart and lung dysfunction in a mouse model of type 2 diabetes (db/db) by reducing oxidative stress, inflammation and pathological remodeling.Pharmacological research · 2016Article
- Deregulation of arginase induces bone complications in high-fat/high-sucrose diet diabetic mouse model.Molecular and cellular endocrinology · 2016Article
- Angiotensin-(1-7) administration benefits cardiac, renal and progenitor cell function in db/db mice.British journal of pharmacology · 2015Article
- Azilsartan, an angiotensin II type 1 receptor blocker, restores endothelial function by reducing vascular inflammation and by increasing the phosphorylation ratio Ser(1177)/Thr(497) of endothelial nitric oxide synthase in diabetic mice.Cardiovascular diabetology · 2014Article
- Alteration of endothelial function markers in women with gestational diabetes and their fetuses.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Diabetics have an increased risk of developing cardiovascular disease, in part due to oxidative stress, resulting in endothelial nitric oxide synthase (eNOS) dysfunction. Studies have demonstrated that angiotensin-(1-7) [Ang-(1-7)] can activate eNOS activity. Because the bone marrow is a primary source of a number of progenitors important in physiological homeostasis and healing, the goal of this study was to evaluate the in vivo effects of Ang-(1-7) treatment on oxidative stress and the ensuing nitrative stress in diabetic bone marrow and its potential pathways. BKS.Cg-Dock7(m) +/+ Lepr(db)/J mice and their heterozygous controls were administered Ang-(1-7) alone or combined with A-779, losartan, PD123,319, nitro-l-arginine methyl ester, or icatibant sc for 14 d. The bone marrow was then collected to measure nitric oxide levels, eNOS phosphorylation, and expression of nitric oxide synthase, superoxide dismutase, and p22-phox. Nitric oxide levels in the bone marrow were significantly decreased in diabetic mice, and Ang-(1-7) treatment was able to significantly increase these measures (P < 0.01). This effect was blocked by the coadministration of PD123,319, A-779, nitro-l-arginine methyl ester, and icatibant. In addition, Ang-(1-7) treatment reversed the paradoxical increase in eNOS and neuronal nitric oxide synthase expression and decreased the phosphorylation of eNOS at Thr495 seen in diabetic mice. Ang-(1-7) also reversed diabetes-induced production of reactive oxygen species by decreasing p22-phox expression and increasing superoxide dismutase 3 expression, leading to a significant reduction in 3-nitrotyrosine formation in diabetic bone marrow (P < 0.05). Our findings demonstrate that Ang-(1-7) administration decreases diabetes-induced oxidative stress in the bone marrow and modifies pathways involved in eNOS dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.