ArticleScientific reports2016
Cardiomyocyte GTP Cyclohydrolase 1 Protects the Heart Against Diabetic Cardiomyopathy.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Declining nitric oxide bioavailability in cardiovascular aging: mechanistic insights and emerging interventions.The journal of cardiovascular aging · 2025Article
- Genetic deletion or pharmacologic inhibition of histone deacetylase 6 protects the heart against ischaemia/reperfusion injury by limiting tumour necrosis factor alpha-induced mitochondrial injury in experimental diabetes.Cardiovascular research · 2024Article
- Ferroptosis: roles and molecular mechanisms in diabetic cardiomyopathy.Frontiers in endocrinology · 2023Review
- SGLT2 Inhibitors: New Hope for the Treatment of Acute Myocardial Infarction?American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022Review
- Tetrahydrobiopterin (BHBiomedicines · 2022Article
- Cardio-omentopexy requires a cardioprotective innate immune response to promote myocardial angiogenesis in mice.JTCVS open · 2022Article
- Exogenous Hydrogen Sulfide Plays an Important Role by Regulating Autophagy in Diabetic-Related Diseases.International journal of molecular sciences · 2021Review
- BH4 Increases nNOS Activity and Preserves Left Ventricular Function in Diabetes.Circulation research · 2021Article
- Identification and analysis of circulating long non-coding RNAs with high significance in diabetic cardiomyopathy.Scientific reports · 2021Article
- Ferroptosis and Its Potential Role in Metabolic Diseases: A Curse or Revitalization?Frontiers in cell and developmental biology · 2021Review
- BH4 activates CaMKK2 and rescues the cardiomyopathic phenotype in rodent models of diabetes.Life science alliance · 2020Article
- Empagliflozin improves post-infarction cardiac remodeling through GTP enzyme cyclohydrolase 1 and irrespective of diabetes status.Scientific reports · 2020Article
- Supplementation of 17β-Estradiol Normalizes Rapid Gastric Emptying by Restoring Impaired Nrf2 and nNOS Function in Obesity-Induced Diabetic Ovariectomized Mice.Antioxidants (Basel, Switzerland) · 2020Article
- The Role of Oxidative Stress in Cardiac Disease: From Physiological Response to Injury Factor.Oxidative medicine and cellular longevity · 2020Review
- Genome-wide differential expression profiling of lncRNAs and mRNAs associated with early diabetic cardiomyopathy.Scientific reports · 2019Article
- Vascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning.Cardiovascular research · 2019Article
- Current status and strategies of long noncoding RNA research for diabetic cardiomyopathy.BMC cardiovascular disorders · 2018Review
- Transgenic overexpression of GTP cyclohydrolase 1 in cardiomyocytes ameliorates post-infarction cardiac remodeling.Scientific reports · 2017Article
- The role of CaDisease models & mechanisms · 2017Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Diabetic cardiomyopathy increases the risk of heart failure and death. At present, there are no effective approaches to preventing its development in the clinic. Here we report that reduction of cardiac GTP cyclohydrolase 1 (GCH1) degradation by genetic and pharmacological approaches protects the heart against diabetic cardiomyopathy. Diabetic cardiomyopathy was induced in C57BL/6 wild-type mice and transgenic mice with cardiomyocyte-specific overexpression of GCH1 with streptozotocin, and control animals were given citrate buffer. We found that diabetes-induced degradation of cardiac GCH1 proteins contributed to adverse cardiac remodeling and dysfunction in C57BL/6 mice, concomitant with decreases in tetrahydrobiopterin, dimeric and phosphorylated neuronal nitric oxide synthase, sarcoplasmic reticulum Ca(2+) handling proteins, intracellular [Ca(2+)]i, and sarcoplasmic reticulum Ca(2+) content and increases in phosphorylated p-38 mitogen-activated protein kinase and superoxide production. Interestingly, GCH-1 overexpression abrogated these detrimental effects of diabetes. Furthermore, we found that MG 132, an inhibitor for 26S proteasome, preserved cardiac GCH1 proteins and ameliorated cardiac remodeling and dysfunction during diabetes. This study deepens our understanding of impaired cardiac function in diabetes, identifies GCH1 as a modulator of cardiac remodeling and function, and reveals a new therapeutic target for diabetic cardiomyopathy.
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