ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Cardiac-specific suppression of NF-κB signaling prevents diabetic cardiomyopathy via inhibition of the renin-angiotensin system.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Progress in the treatment of diabetic cardiomyopathy, a systematic review.Pharmacology research & perspectives · 2024Pooled it
- Inflammatory signalling in diabetic cardiomyopathy: molecular mechanisms and potential therapeutic strategies.Nature reviews. Cardiology · 2026Review
- Diabetic Atrial Cardiomyopathy: Pathogenesis, Diagnosis, Management, AI-Driven Diagnosis, and Risk Prediction.Journal of diabetes research · 2026Review
- Expression of the Renin-Angiotensin System in the Heart, Aorta, and Perivascular Adipose Tissue in an Animal Model of Type 1 Diabetes.International journal of molecular sciences · 2025Article
- REDD1 Deletion Suppresses NF-κB Signaling in Cardiomyocytes and Prevents Deficits in Cardiac Function in Diabetic Mice.International journal of molecular sciences · 2024Article
- Electrocardiographic and histopathological characterizations of diabetic cardiomyopathy in rats.Environmental science and pollution research international · 2022Article
- The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction.Bioengineered · 2021Article
- Pgc-1α Promotes Phosphorylation, Inflammation, and Apoptosis in H9c2 Cells During the Early Stage of Lipopolysaccharide Induction.Inflammation · 2021Article
- Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response.Frontiers in physiology · 2021Review
- Cardioprotective role of GTS-21 by attenuating the TLR4/NF-κB pathway in streptozotocin-induced diabetic cardiomyopathy in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Senescence and Type 2 Diabetic Cardiomyopathy: How Young Can You Die of Old Age?Frontiers in pharmacology · 2021Review
- Inflammation in Metabolic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- Changes of Necroptosis in Irbesartan Medicated Cardioprotection in Diabetic Rats.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Cardioprotective effects of polydatin against myocardial injury in diabetic rats via inhibition of NADPH oxidase and NF-κB activities.BMC complementary medicine and therapies · 2020Article
- Mechanisms of diabetic cardiomyopathy and potential therapeutic strategies: preclinical and clinical evidence.Nature reviews. Cardiology · 2020Review
- Silencing of ATP2B1-AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA-mediated NF-κB signalling pathway.Journal of cellular and molecular medicine · 2020Article
- [Expression of NLRP1 inflammasomes in myocardial tissue of diabetic rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Liquiritigenin-Loaded Submicron Emulsion Protects Against Doxorubicin-Induced Cardiotoxicity via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activity.International journal of nanomedicine · 2020Article
- High-glucose-induced apoptosis, ROS production and pro-inflammatory response in cardiomyocytes is attenuated by metformin treatment via PP2A activation.Journal of biosciences · 2020Article
- IL-1β and Statin Treatment in Patients with Myocardial Infarction and Diabetic Cardiomyopathy.Journal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Activation of NF-κB signaling in the heart may be protective or deleterious depending on the pathological context. In diabetes, the role of NF-κB in cardiac dysfunction has been investigated using pharmacological approaches that have a limitation of being nonspecific. Furthermore, the specific cellular pathways by which NF-κB modulates heart function in diabetes have not been identified. To address these questions, we used a transgenic mouse line expressing mutated IκB-α in the heart (3M mice), which prevented activation of canonical NF-κB signaling. Diabetes was developed by streptozotocin injections in wild-type (WT) and 3M mice. Diabetic WT mice developed systolic and diastolic cardiac dysfunction by the 12th week, as measured by echocardiography. In contrast, cardiac function was preserved in 3M mice up to 24 wk of diabetes. Diabetes induced an elevation in cardiac oxidative stress in diabetic WT mice but not 3M mice compared with nondiabetic control mice. In diabetic WT mice, an increase in the phospholamban/sarco(endo)plasmic reticulum Ca(2+)-ATPase 2 ratio and decrease in ryanodine receptor expression were observed, whereas diabetic 3M mice showed an opposite effect on these parameters of Ca(2+) handling. Significantly, renin-angiotensin system activity was suppressed in diabetic 3M mice compared with an increase in WT animals. In conclusion, these results demonstrate that inhibition of NF-κB signaling in the heart prevents diabetes-induced cardiac dysfunction through preserved Ca(2+) handling and inhibition of the cardiac renin-angiotensin system.
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