ArticleProceedings of the National Academy of Sciences of the United States of America2010
Lack of both bradykinin B1 and B2 receptors enhances nephropathy, neuropathy, and bone mineral loss in Akita diabetic mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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58 citing papers in PubMed, 121 citations in OpenAlex.
- Long-chain polyphosphates induce glomerular microthrombi and exacerbate LPS-induced acute kidney injury in mouse.Disease models & mechanisms · 2026Article
- Bradykinin-bradykinin 2 receptor and oxidative stress.Annals of medicine · 2025Review
- Dextran sodium sulfate-induced colitis in male BALB/c mice leads to albuminuria and increased markers of inflammation and tissue damage in the kidney.Physiological reports · 2025Article
- Deletion of kinin receptor B2 enhances orthodontic tooth movement and alveolar bone remodeling.PloS one · 2025Article
- Shared signaling pathways and comprehensive therapeutic approaches among diabetes complications.Frontiers in medicine · 2024Review
- Rodent models to study type 1 and type 2 diabetes induced human diabetic nephropathy.Molecular biology reports · 2023Review
- Kinin receptors regulate skeletal muscle regeneration: differential effects for B1 and B2 receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Acute kidney injury caused by venomous animals: inflammatory mechanisms.The journal of venomous animals and toxins including tropical diseases · 2021Article
- PodocyteFrontiers in pharmacology · 2021Article
- Role of Kinins in Hypertension and Heart Failure.Pharmaceuticals (Basel, Switzerland) · 2020Review
- High molecular weight kininogen contributes to early mortality and kidney dysfunction in a mouse model of sickle cell disease.Journal of thrombosis and haemostasis : JTH · 2020Article
- Revisiting Experimental Models of Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- The kallikrein-kinin pathway as a mechanism for auto-control of brown adipose tissue activity.Nature communications · 2020Article
- Innate immunity in diabetic kidney disease.Nature reviews. Nephrology · 2020Review
- Pancreatic kallikrein protects against diabetic retinopathy in KK Cg-ADiabetologia · 2019Article
- Renal and vascular effects of kallikrein inhibition in a model of Lonomia obliqua venom-induced acute kidney injury.PLoS neglected tropical diseases · 2019Article
- Inflammation and Immunity Pathways Regulate Genetic Susceptibility to Diabetic Nephropathy.Diabetes · 2018Article
- The investigation of association between IL-1Ra and ACE I/D polymorphisms in carpal tunnel syndrome.Journal of clinical laboratory analysis · 2018Article
- Susceptible and Prognostic Genetic Factors Associated with Diabetic Peripheral Neuropathy: A Comprehensive Literature Review.International journal of endocrinology · 2018Review
- Plasma bradykinin and early diabetic nephropathy lesions in type 1 diabetes mellitus.PloS one · 2017Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
An insertion polymorphism of the angiotensin-I converting enzyme gene (ACE) is common in humans and the higher expressing allele is associated with an increased risk of diabetic complications. The ACE polymorphism does not significantly affect blood pressure or angiotensin II levels, suggesting that the kallikrein-kinin system partly mediates the effects of the polymorphism. We have therefore explored the influence of lack of both bradykinin receptors (B1R and B2R) on diabetic nephropathy, neuropathy, and osteopathy in male mice heterozygous for the Akita diabetogenic mutation in the insulin 2 gene (Ins2). We find that all of the detrimental phenotypes observed in Akita diabetes are enhanced by lack of both B1R and B2R, including urinary albumin excretion, glomerulosclerosis, glomerular basement membrane thickening, mitochondrial DNA deletions, reduction of nerve conduction velocities and of heat sensation, and bone mineral loss. Absence of the bradykinin receptors also enhances the diabetes-associated increases in plasma thiobarbituric acid-reactive substances, mitochondrial DNA deletions, and renal expression of fibrogenic genes, including transforming growth factor beta1, connective tissue growth factor, and endothelin-1. Thus, lack of B1R and B2R exacerbates diabetic complications. The enhanced renal injury in diabetic mice caused by lack of B1R and B2R may be mediated by a combination of increases in oxidative stress, mitochondrial DNA damage and over expression of fibrogenic genes.
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