ArticleBiochemical and biophysical research communications2010
Attenuation of beta2-adrenergic receptors and homocysteine metabolic enzymes cause diabetic cardiomyopathy.
Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Emerging Insights into the Relationship Between Amino Acid Metabolism and Diabetic Cardiomyopathy.Biomolecules · 2025Review
- Homocysteine as a Predictor of Paroxysmal Atrial Fibrillation-Related Events: A Scoping Review of the Literature.Diagnostics (Basel, Switzerland) · 2022Article
- Different Pattern of Cardiovascular Impairment in Methylmalonic Acidaemia Subtypes.Frontiers in pediatrics · 2022Article
- Heart failure in diabetes.Metabolism: clinical and experimental · 2021Review
- Review
- Association between Beta2-Adrenergic Receptor Agonists and the Risk of Vascular Complications in Diabetic Patients: A Population-Based Cohort Study.Journal of clinical medicine · 2019Article
- Hydrogen sulfide-mediated regulation of cell death signaling ameliorates adverse cardiac remodeling and diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2019Review
- Hydrogen Sulfide Ameliorates Homocysteine-Induced Cardiac Remodeling and Dysfunction.Frontiers in physiology · 2019Article
- Transgenic Expression of miR-133a in the Diabetic Akita Heart Prevents Cardiac Remodeling and Cardiomyopathy.Frontiers in cardiovascular medicine · 2019Article
- The present and future role of ultrasound targeted microbubble destruction in preclinical studies of cardiac gene therapy.Journal of thoracic disease · 2018Review
- MiR-133a Mimic Alleviates T1DM-Induced Systolic Dysfunction in Akita: An MRI-Based Study.Frontiers in physiology · 2018Article
- Folic acid prevents cardiac dysfunction and reduces myocardial fibrosis in a mouse model of high-fat diet-induced obesity.Nutrition & metabolism · 2017Article
- Cardiac transcriptome profiling of diabetic Akita mice using microarray and next generation sequencing.PloS one · 2017Article
- Article
- Ablation of Matrix Metalloproteinase-9 Prevents Cardiomyocytes Contractile Dysfunction in Diabetics.Frontiers in physiology · 2016Article
- Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes.Molecular and cellular biochemistry · 2015Article
- Differential expression of dicer, miRNAs, and inflammatory markers in diabetic Ins2+/- Akita hearts.Cell biochemistry and biophysics · 2014Article
- Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: role of Ca2+/calmodulin-activated protein kinase II.Free radical biology & medicine · 2013Article
- Predictors and prevention of diabetic cardiomyopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2013Article
- MicroRNA-133a regulates DNA methylation in diabetic cardiomyocytes.Biochemical and biophysical research communications · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Although adrenergic receptors (AR) and hyperhomocysteinemia (HHcy) are implicated in heart failure, their role in diabetic cardiomyopathy is not completely understood. We tested the hypothesis that glucose mediated depletion of beta2-AR and HHcy impair contractile function of cardiomyocytes leading to diabetic cardiomyopathy. To prove the hypothesis, cardiac function was assessed in 12week male diabetic Ins2+/- Akita and C57BL/6J mice by echocardiography, pressure-volume loop, and contractile function of cardiomyocytes. The results revealed cardiac dysfunction in Akita. To investigate the mechanism, the levels of beta2-AR, GLUT4, sarcoplasmic reticulum calcium ATP-ase-isoform 2 (SERCA-2) and homocysteine (Hcy) metabolic enzymes-cystathionine beta synthase (CBS), cystathionine gamma lyase (CTH), and methyl tetrahydrofolate reductase (MTHFR) were determined in the heart. It revealed down-regulation of beta2-AR, GLUT4, SERCA-2, CBS, CTH, and MTHFR in Akita. Attenuation of beta2-AR in hyperglycemic condition was also confirmed in cardiomyocytes at in vitro level. Interestingly, the ex vivo treatment of cardiomyocytes with beta2-AR antagonist deteriorated whereas beta-AR agonist ameliorated contractile function. It points to the involvement of beta2-AR in diabetic cardiomyopathy. We conclude that degradation of beta2-AR and impairment of Hcy metabolism is implicated in diabetic cardiomyopathy.
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