ArticleDiabetologia2012
Enhanced phosphoinositide 3-kinase(p110α) activity prevents diabetes-induced cardiomyopathy and superoxide generation in a mouse model of diabetes.
Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- A systematic review of fetal genes as biomarkers of cardiac hypertrophy in rodent models of diabetes.PloS one · 2014Pooled it
- Understanding Exercise-induced Protection in Heart Failure with Reduced Ejection Fraction and Heart Failure with Preserved Ejection Fraction: Molecular Mechanisms and New Therapeutic Opportunities.Cardiac failure review · 2026Review
- Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026Review
- Guidelines for diet-induced models of cardiometabolic syndrome.American journal of physiology. Heart and circulatory physiology · 2025Review
- Generation and evaluation of a novel PI3K-targeting gene therapy in the failing mouse heart and healthy sheep heart.Journal of molecular and cellular cardiology plus · 2025Article
- New frontiers in type I diabetes treatment: the impact of mesenchymal stromal cells on long-term complications.Frontiers in clinical diabetes and healthcare · 2025Review
- Distinct functional and molecular profiles between physiological and pathological atrial enlargement offer potential new therapeutic opportunities for atrial fibrillation.Clinical science (London, England : 1979) · 2024Article
- The double burden: type 1 diabetes and heart failure-a comprehensive review.Cardiovascular diabetology · 2024Review
- A gene therapy targeting medium-chain acyl-CoA dehydrogenase (MCAD) did not protect against diabetes-induced cardiac pathology.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Deletion of the muscle enriched lncRNA Oip5os1 induces atrial dysfunction in male mice with diabetes.Physiological reports · 2023Article
- Phenolics Extracted fromMolecules (Basel, Switzerland) · 2023Article
- Ferroptosis, necroptosis and cuproptosis: Novel forms of regulated cell death in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- Article
- Signaling Pathways Related to Oxidative Stress in Diabetic Cardiomyopathy.Frontiers in endocrinology · 2022Review
- IGF1-PI3K-induced physiological cardiac hypertrophy: Implications for new heart failure therapies, biomarkers, and predicting cardiotoxicity.Journal of sport and health science · 2021Review
- Rg1 protects H9C2 cells from high glucose-/palmitate-induced injury via activation of AKT/GSK-3β/Nrf2 pathway.Journal of cellular and molecular medicine · 2020Article
- The Peroxisome Proliferator-Activated Receptor-Gamma Coactivator-1α-Heme Oxygenase 1 Axis, a Powerful Antioxidative Pathway with Potential to Attenuate Diabetic Cardiomyopathy.Antioxidants & redox signaling · 2020Review
- Basic Mechanisms of Diabetic Heart Disease.Circulation research · 2020Review
- Annexin-A1 deficiency exacerbates pathological remodelling of the mesenteric vasculature in insulin-resistant, but not insulin-deficient, mice.British journal of pharmacology · 2020Article
- Defining the Progression of Diabetic Cardiomyopathy in a Mouse Model of Type 1 Diabetes.Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisDiabetic cardiomyopathy is characterised by diastolic dysfunction, oxidative stress, fibrosis, apoptosis and pathological cardiomyocyte hypertrophy. Phosphoinositide 3-kinase (PI3K)(p110α) is a cardioprotective kinase, but its role in the diabetic heart is unknown. The aim of this study was to assess whether PI3K(p110α) plays a critical role in the induction of diabetic cardiomyopathy, and whether increasing PI3K(p110α) activity in the heart can prevent the development of cardiac dysfunction in a setting of diabetes.
methodsType 1 diabetes was induced with streptozotocin in adult male cardiac-specific transgenic mice with increased PI3K(p110α) activity (constitutively active PI3K [p110α], caPI3K] or decreased PI3K(p110α) activity (dominant-negative PI3K [p110α], dnPI3K) and non-transgenic (Ntg) mice for 12 weeks. Cardiac function, histological and molecular analyses were performed.
resultsDiabetic Ntg mice displayed diastolic dysfunction and increased cardiomyocyte size, expression of atrial and B-type natriuretic peptides (Anp, Bnp), fibrosis and apoptosis, as well as increased superoxide generation and increased protein kinase C β2 (PKCβ2), p22 ( phox ) and apoptosis signal-regulating kinase 1 (Ask1) expression. Diabetic dnPI3K mice displayed an exaggerated cardiomyopathy phenotype compared with diabetic Ntg mice. In contrast, diabetic caPI3K mice were protected against diastolic dysfunction, pathological cardiomyocyte hypertrophy, fibrosis and apoptosis. Protection in diabetic caPI3K mice was associated with attenuation of left ventricular superoxide generation, attenuated Anp, Bnp, PKCβ2, Ask1 and p22 ( phox ) expression, and elevated AKT. Further, in cardiomyocyte-like cells, increased PI3K(p110α) activity suppressed high glucose-induced superoxide generation and enhanced mitochondrial function. CONCLUSIONS/
interpretationThese results demonstrate that reduced PI3K activity accelerates the development of diabetic cardiomyopathy, and that enhanced PI3K(p110α) activity can prevent adverse cardiac remodelling and dysfunction in a setting of diabetes.
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