ArticleDiabetes2010
Cardiac-specific IGF-1 receptor transgenic expression protects against cardiac fibrosis and diastolic dysfunction in a mouse model of diabetic cardiomyopathy.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
71 citing papers in PubMed, 145 citations in OpenAlex.
- [Liraglutide improves cardiac structure and function in mice with advanced diabetic nephropathy and massive proteinuria].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Intersecting Molecular Pathways in Cardiovascular Disease and Diabetes Mellitus: Emerging Roles of Inflammation and Therapeutics.Diabetes/metabolism research and reviews · 2026Review
- A bibliometric analysis of myocardial fibrosis in diabetic cardiomyopathy: global trends and future directions.Journal of cardiothoracic surgery · 2026Article
- 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
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Inhibition of the Renin-Angiotensin System Improves Hemodynamic Function of the Diabetic Rat Heart by Restoring Intracellular Calcium Regulation.Biomedicines · 2025Article
- Genistein Enhances the Beneficial Effects of Exercise on Antioxidant and Anti-inflammatory Balance and Cardiomyopathy in Ovariectomized Diabetic Rats.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2025Article
- Diminished levels of insulin-like growth factor-1 may be a risk factor for peripheral neuropathy in type 2 diabetes patients.Journal of diabetes investigation · 2024Article
- 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
- Compromised diabetic heart function is not affected by miR-378a upregulation upon hyperglycemia.Pharmacological reports : PR · 2023Article
- Microvascular Myocardial Ischemia in Patients With Diabetes Without Obstructive Coronary Stenosis and Its Association With Angina.Korean journal of radiology · 2023Article
- Epigenomic signature of major congenital heart defects in newborns with Down syndrome.Human genomics · 2023Article
- Insulin-Like Growth Factor 1 Receptor Deficiency Alleviates Angiotensin II-Induced Cardiac Fibrosis Through the Protein Kinase B/Extracellular Signal-Regulated Kinase/Nuclear Factor-κB Pathway.Journal of the American Heart Association · 2023Article
- Epigenomic signature of major congenital heart defects in newborns with Down syndrome.medRxiv : the preprint server for health sciences · 2023Article
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Chrysin-based supramolecular cyclodextrin-calixarene drug delivery system: a novel approach for attenuating cardiac fibrosis in chronic diabetes.Frontiers in pharmacology · 2023Article
- Zuogui Jiangtang Shuxin formula Ameliorates diabetic cardiomyopathy miceFrontiers in endocrinology · 2023Article
- Article
- SIRPα Mediates IGF1 Receptor in Cardiomyopathy Induced by Chronic Kidney Disease.Circulation research · 2022Article
- IGF-1 protects against angiotensin II-induced cardiac fibrosis by targeting αSMA.Cell death & disease · 2021Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCompelling epidemiological and clinical evidence has identified a specific cardiomyopathy in diabetes, characterized by early diastolic dysfunction and adverse structural remodeling. Activation of the insulin-like growth factor 1 (IGF-1) receptor (IGF-1R) promotes physiological cardiac growth and enhances contractile function. The aim of the present study was to examine whether cardiac-specific overexpression of IGF-1R prevents diabetes-induced myocardial remodeling and dysfunction associated with a murine model of diabetes. RESEARCH DESIGN AND
methodsType 1 diabetes was induced in 7-week-old male IGF-1R transgenic mice using streptozotocin and followed for 8 weeks. Diastolic and systolic function was assessed using Doppler and M-mode echocardiography, respectively, in addition to cardiac catheterization. Cardiac fibrosis and cardiomyocyte width, heart weight index, gene expression, Akt activity, and IGF-1R protein content were also assessed.
resultsNontransgenic (Ntg) diabetic mice had reduced initial (E)-to-second (A) blood flow velocity ratio (E:A ratio) and prolonged deceleration times on Doppler echocardiography compared with nondiabetic counterparts, indicative markers of diastolic dysfunction. Diabetes also increased cardiomyocyte width, collagen deposition, and prohypertrophic and profibrotic gene expression compared with Ntg nondiabetic littermates. Overexpression of the IGF-1R transgene markedly reduced collagen deposition, accompanied by a reduction in the incidence of diastolic dysfunction. Akt phosphorylation was elevated approximately 15-fold in IGF-1R nondiabetic mice compared with Ntg, and this was maintained in a setting of diabetes.
conclusionsThe current study suggests that cardiac overexpression of IGF-1R prevented diabetes-induced cardiac fibrosis and diastolic dysfunction. Targeting IGF-1R-Akt signaling may represent a therapeutic target for the treatment of diabetic cardiac disease.
Indexed as
Identifiers
What OpenQuestion holds
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.