ArticleThe Journal of physiology2007
Carbonic anhydrase inhibition prevents and reverts cardiomyocyte hypertrophy.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 78 citations in OpenAlex.
- GEO combined with quantitative protein trait loci identify causative proteins in hypertrophic cardiomyopathy.ESC heart failure · 2025Article
- Naringin attenuates angiotensin II induced cardiac hypertrophy by inhibiting carbonic anhydrase II.Scientific reports · 2025Article
- CRISPRi/a screens in human iPSC-cardiomyocytes identify glycolytic activation as a druggable target for doxorubicin-induced cardiotoxicity.Cell stem cell · 2024Article
- USP20 deletion promotes eccentric cardiac remodeling in response to pressure overload and increases mortality.American journal of physiology. Heart and circulatory physiology · 2024Article
- The insulin receptor family in the heart: new light on old insights.Bioscience reports · 2022Review
- The HVCN1 voltage-gated proton channel contributes to pH regulation in canine ventricular myocytes.The Journal of physiology · 2022Article
- Myocardial and mitochondrial effects of the anhydrase carbonic inhibitor ethoxzolamide in ischemia-reperfusion.Physiological reports · 2021Article
- Carbonic anhydrase IX and hypoxia-inducible factor 1 attenuate cardiac dysfunction after myocardial infarction.Pflugers Archiv : European journal of physiology · 2021Article
- The insulin receptor family and protein kinase B (Akt) are activated in the heart by alkaline pH and α1-adrenergic receptors.The Biochemical journal · 2021Article
- Bone marrow-derived mesenchymal stem cells attenuate myocardial ischemia-reperfusion injury via upregulation of splenic regulatory T cells.BMC cardiovascular disorders · 2021Article
- The therapeutic importance of acid-base balance.Biochemical pharmacology · 2021Review
- Acetazolamide Improves Right Ventricular Function and Metabolic Gene Dysregulation in Experimental Pulmonary Arterial Hypertension.Frontiers in cardiovascular medicine · 2021Article
- Carbonic anhydrase IX and acid transport in cancer.British journal of cancer · 2020Review
- Transgenic expression of carbonic anhydrase III in cardiac muscle demonstrates a mechanism to tolerate acidosis.American journal of physiology. Cell physiology · 2019Article
- Review
- RNA SEQ Analysis Indicates that the AE3 ClScientific reports · 2017Article
- Bioactive Natural Product and Superacid Chemistry for Lead Compound Identification: A Case Study of Selective hCA III and L-Type CaMolecules (Basel, Switzerland) · 2017Review
- Functional interaction between bicarbonate transporters and carbonic anhydrase modulates lactate uptake into mouse cardiomyocytes.Pflugers Archiv : European journal of physiology · 2015Article
- New insights into carbonic anhydrase inhibition, vasodilation, and treatment of hypertensive-related diseases.Current hypertension reports · 2014Review
- Critical role of bicarbonate and bicarbonate transporters in cardiac function.World journal of biological chemistry · 2014Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyocyte growth contributes substantially to the progression of heart failure. Activation of the plasma membrane Na+-H+ exchanger (NHE1) and Cl- -HCO3- exchanger (AE3) has emerged as a central point in the hypertrophic cascade. Both NHE1 and AE3 bind carbonic anhydrase (CA), which activates their transport flux, by providing H+ and HCO3-, their respective transport substrates. We examined the contribution of CA activity to the hypertrophic response of cultured neonatal and adult rodent cardiomyocytes. Phenylephrine (PE) increased cell size by 37 +/- 2% and increased expression of the hypertrophic marker, atrial natriuretic factor mRNA, twofold in cultured neonatal rat cardiomyocytes. Cell size was also increased in adult cardiomyocytes subjected to angiotensin II or PE treatment. These effects were associated with increased expression of cytosolic CAII protein and the membrane-anchored isoform, CAIV. The membrane-permeant CA inhibitor, 6-ethoxyzolamide (ETZ), both prevented and reversed PE-induced hypertrophy in a concentration-dependent manner in neonate cardiomyocytes (IC50=18 microm). ETZ and the related CA inhibitor methazolamide prevented hypertrophy in adult cardiomyocytes. In addition, ETZ inhibited transport activity of NHE1 and the AE isoform, AE3, with respective EC50 values of 1.2 +/- 0.3 microm and 2.7 +/- 0.3 microm. PE significantly increased neonatal cardiomyocyte Ca2+ transient frequency from 0.33 +/- 0.4 Hz to 0.77 +/- 0.04 Hz following 24 h treatment; these Ca2+ -handling abnormalities were completely prevented by ETZ (0.28 +/- 0.07 Hz). Our study demonstrates a novel role for CA in mediating the hypertrophic response of cardiac myocytes to PE and suggests that CA inhibition represents an effective therapeutic approach towards mitigation of the hypertrophic phenotype.
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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.