ArticleJournal of the American Heart Association2014
Carbonic anhydrase activation is associated with worsened pathological remodeling in human ischemic diabetic cardiomyopathy.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 103 citations in OpenAlex.
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- Aqueous carbonic anhydrase-1 overexpression and its association with cytokine profiles and macular structural changes in retinal vein occlusion-associated macular edema.Scientific reports · 2025Article
- Multi-Target Glitazones for Modulating Peroxisome Proliferator-Activated Receptor-γ, Cyclooxygenase-2, and Carbonic Anhydrases for the Management of Metabolic Dysfunction.ACS pharmacology & translational science · 2025Article
- Comparison of the proteomic landscape in experimental ischemia reperfusion with versus without ischemic preconditioning.Scientific reports · 2025Article
- Navigating the Neuroimmunomodulation Frontier: Pioneering Approaches and Promising Horizons-A Comprehensive Review.International journal of molecular sciences · 2024Review
- Cardiometabolic biomarker patterns associated with cardiac MRI defined fibrosis and microvascular dysfunction in patients with heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2024Article
- Transcriptomics data integration and analysis to uncover hallmark genes in hypertrophic cardiomyopathy.American journal of translational research · 2024Article
- Proteomics and Precise Exercise Phenotypes in Heart Failure With Preserved Ejection Fraction: A Pilot Study.Journal of the American Heart Association · 2023Article
- Cellular senescence and the blood-brain barrier: Implications for aging and age-related diseases.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Maternal DNA methylation signatures of arsenic exposure is associated with adult offspring insulin resistance in the Strong Heart Study.Environment international · 2023Article
- Endothelial Dysfunction, Erectile Deficit and Cardiovascular Disease: An Overview of the Pathogenetic Links.Biomedicines · 2022Review
- Endothelial Microparticles as Potential Biomarkers in the Assessment of Endothelial Dysfunction in Hypercholesterolemia.Medicina (Kaunas, Lithuania) · 2022Article
- Article
- Changes in extracellular matrix in failing human non-ischemic and ischemic hearts with mechanical unloading.Journal of molecular and cellular cardiology · 2022Article
- Unraveling and Targeting Myocardial Regeneration Deficit in Diabetes.Antioxidants (Basel, Switzerland) · 2022Review
- MicroRNAs as the Potential Regulators of SARS-CoV-2 Infection and Modifiers of the COVID-19 Clinical Features.Molecular biology · 2022Article
- Regulating Polyamine Metabolism by miRNAs in Diabetic Cardiomyopathy.Current diabetes reports · 2021Review
- Plasma BDNF and Cytokines Correlated with Protein Biomarkers for Bipolar II Disorder.Journal of personalized medicine · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetes mellitus (DM) has multifactorial detrimental effects on myocardial tissue. Recently, carbonic anhydrases (CAs) have been shown to play a major role in diabetic microangiopathy but their role in the diabetic cardiomyopathy is still unknown. METHODS AND
resultsWe obtained left ventricular samples from patients with DM type 2 (DM-T2) and nondiabetic (NDM) patients with postinfarct heart failure who were undergoing surgical coronary revascularization. Myocardial levels of CA-I and CA-II were 6- and 11-fold higher, respectively, in DM-T2 versus NDM patients. Elevated CA-I expression was mainly localized in the cardiac interstitium and endothelial cells. CA-I induced by high glucose levels hampers endothelial cell permeability and determines endothelial cell apoptosis in vitro. Accordingly, capillary density was significantly lower in the DM-T2 myocardial samples (mean±SE=2152±146 versus 4545±211/mm(2)). On the other hand, CA-II was mainly upregulated in cardiomyocytes. The latter was associated with sodium-hydrogen exchanger-1 hyperphosphorylation, exaggerated myocyte hypertrophy (cross-sectional area 565±34 versus 412±27 μm(2)), and apoptotic death (830±54 versus 470±34 per 10(6) myocytes) in DM-T2 versus NDM patients. CA-II is activated by high glucose levels and directly induces cardiomyocyte hypertrophy and death in vitro, which are prevented by sodium-hydrogen exchanger-1 inhibition. CA-II was shown to be a direct target for repression by microRNA-23b, which was downregulated in myocardial samples from DM-T2 patients. MicroRNA-23b is regulated by p38 mitogen-activated protein kinase, and it modulates high-glucose CA-II-dependent effects on cardiomyocyte survival in vitro.
conclusionsMyocardial CA activation is significantly elevated in human diabetic ischemic cardiomyopathy. These data may open new avenues for targeted treatment of diabetic heart failure.
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