ArticleProceedings of the National Academy of Sciences of the United States of America2004
Mice with cardiomyocyte-specific disruption of the endothelin-1 gene are resistant to hyperthyroid cardiac hypertrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 85 citations in OpenAlex.
- Urinary clusterin as a biomarker of human kidney disease progression and response to the endothelin receptor antagonist atrasentan: An exploratory analysis from the SONAR trial.Nature communications · 2026Trial
- Podocyte-derived endothelin-1 and endothelial cell endothelin A receptors are essential for glomerular injury in mouse models of focal segmental glomerulosclerosis.Kidney international · 2026Article
- Progenitor-derived endothelin controls dermal sheath contraction for hair follicle regression.Nature cell biology · 2023Article
- High triiodothyronine levels induce myocardial hypertrophy via BAFF overexpression.Journal of cellular and molecular medicine · 2022Article
- Endothelial Dysfunction in Heart Failure With Preserved Ejection Fraction: What are the Experimental Proofs?Frontiers in physiology · 2022Review
- Vezf1 regulates cardiac structure and contractile function.EBioMedicine · 2020Article
- Cardiomyokines from the heart.Cellular and molecular life sciences : CMLS · 2018Review
- Plasma endothelin-1 levels are increased in atrial fibrillation patients with hyperthyroidism.PloS one · 2018Article
- T cells upon activation promote endothelin 1 production in monocytes via IFN-γ and TNF-α.Scientific reports · 2017Article
- Enhanced endothelin-1/Rho-kinase signalling and coronary microvascular dysfunction in hypertensive myocardial hypertrophy.Cardiovascular research · 2017Article
- Mechanistic Systems Modeling to Improve Understanding and Prediction of Cardiotoxicity Caused by Targeted Cancer Therapeutics.Frontiers in physiology · 2017Article
- Endothelin.Pharmacological reviews · 2016Review
- The Effect of Sorafenib, Tadalafil and Macitentan Treatments on Thyroxin-Induced Hemodynamic Changes and Cardiac Abnormalities.PloS one · 2016Article
- Cre recombinase-regulated Endothelin1 transgenic mouse lines: novel tools for analysis of embryonic and adult disorders.Developmental biology · 2015Article
- Higher circulatory level of endothelin-1 in hypertensive subjects screened through a cross-sectional study of rural Bangladeshi women.Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation.Cell journal · 2015Article
- Article
- Vascular endothelium derived endothelin-1 is required for normal heart function after chronic pressure overload in mice.PloS one · 2014Article
- Endothelin antagonism and its role in the treatment of hypertension.Current hypertension reports · 2013Review
- Endothelin-2 deficiency causes growth retardation, hypothermia, and emphysema in mice.The Journal of clinical investigation · 2013Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Endothelin 1 (ET-1), a potent vasoconstrictor peptide expressed by endothelium, is also produced in the heart in response to a variety of stresses. It induces hypertrophy in cultured cardiac myocytes but only at concentrations far greater than those found in plasma. We tested whether ET-1 generated by cardiac myocytes in vivo is a local signal for cardiac hypertrophy. To avoid the perinatal lethality seen in systemic ET-1-null mice, we used the Cre/loxP system to generate mice with cardiac myocyte-specific disruption of the ET-1 gene. We used the alpha-myosin heavy chain promoter to drive expression of Cre and were able to obtain 75% reduction in ET-1 mRNA in cardiac myocytes isolated from these mice at baseline and after stimulation, in vivo, for 24 h with tri-iodothyronine (T3). Necropsy measurements of cardiac mass indexed for body weight showed a 57% reduction in cardiac hypertrophy in response to 16 days of exogenous T3 in mice homozygous for the disrupted ET-1 allele compared to siblings with an intact ET-1 gene. Moreover, in vivo MRI showed only a 3% increase in left ventricular mass indexed for body weight in mice with the disrupted allele after 3 weeks of T3 treatment versus a 27% increase in mice with an intact ET-1 gene. A reduced hypertrophic response was confirmed by planimetry of cardiac myocytes. We conclude that ET-1, produced locally by cardiac myocytes, and acting in a paracrine/autocrine manner, is an important signal for myocardial hypertrophy that facilitates the response to thyroid hormone.
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