ArticleDiabetes2009
Gene deletion of the kinin receptor B1 attenuates cardiac inflammation and fibrosis during the development of experimental diabetic cardiomyopathy.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 113 citations in OpenAlex.
- Effect of high glucose on the gene expression profiling in cardiac fibroblasts from rats at different ages.PeerJ · 2025Article
- Transient receptor potential vanilloid type 1: cardioprotective effects in diabetic models.Channels (Austin, Tex.) · 2023Review
- Kinins: Locally formed peptides during inflammation with potential use in tissue regeneration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Genetic Ablation and Pharmacological Blockade of Bradykinin B1 Receptor Unveiled a Detrimental Role for the Kinin System in Chagas Disease Cardiomyopathy.Journal of clinical medicine · 2023Article
- Kinin B1 receptor blockade attenuates hepatic fibrosis and portal hypertension in chronic liver diseases in mice.Journal of translational medicine · 2022Article
- Bibliometric analysis of the inflammation in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Reversal of pulmonary arterial hypertension and neointimal formation by kinin B1 receptor blockade.Respiratory research · 2021Article
- Review
- What would Sérgio Ferreira say to your physician in this war against COVID-19: How about kallikrein/kinin system?Medical hypotheses · 2020Article
- Differential Expression of Kinin Receptors in Human Wet and Dry Age-Related Macular Degeneration Retinae.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Effect and Mechanism ofDiabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Article
- Tanshinone IIA ameliorates diabetic cardiomyopathy by inhibiting Grp78 and CHOP expression in STZ-induced diabetes rats.Experimental and therapeutic medicine · 2019Article
- Functional variant of the carboxypeptidase M (CPM) gene may affect silica-related pneumoconiosis susceptibility by its expression: a multistage case-control study.Occupational and environmental medicine · 2019Article
- Sophocarpine Suppresses NF-κB-Mediated Inflammation BothFrontiers in pharmacology · 2019Article
- The Effects of Bradykinin B1 Receptor Antagonism on the Myocardial and Vascular Consequences of Hypertension in SHR Rats.Frontiers in physiology · 2019Article
- Carvedilol alleviates diabetic cardiomyopathy in diabetic rats.Experimental and therapeutic medicine · 2019Article
- Profile of cardiac lipid metabolism in STZ-induced diabetic mice.Lipids in health and disease · 2018Article
- Baicalein Protects Rats with Diabetic Cardiomyopathy Against Oxidative Stress and Inflammation Injury via Phosphatidylinositol 3-Kinase (PI3K)/AKT Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway.International journal of molecular medicine · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDiabetic cardiomyopathy is associated with increased mortality in patients with diabetes. The underlying pathology of this disease is still under discussion. We studied the role of the kinin B1 receptor on the development of experimental diabetic cardiomyopathy. RESEARCH DESIGN AND
methodsWe utilized B1 receptor knockout mice and investigated cardiac inflammation, fibrosis, and oxidative stress after induction of streptozotocin (STZ)-induced diabetes. Furthermore, the left ventricular function was measured by pressure-volume loops after 8 weeks of diabetes.
resultsB1 receptor knockout mice showed an attenuation of diabetic cardiomyopathy with improved systolic and diastolic function in comparison with diabetic control mice. This was associated with a decreased activation state of the mitogen-activated protein kinase p38, less oxidative stress, as well as normalized cardiac inflammation, shown by fewer invading cells and no increase in matrix metalloproteinase-9 as well as the chemokine CXCL-5. Furthermore, the profibrotic connective tissue growth factor was normalized, leading to a reduction in cardiac fibrosis despite severe hyperglycemia in mice lacking the B1 receptor.
conclusionsThese findings suggest that the B1 receptor is detrimental in diabetic cardiomyopathy in that it mediates inflammatory and fibrotic processes. These insights might have useful implications on future studies utilizing B1 receptor antagonists for treatment of human diabetic cardiomyopathy.
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