ArticlePloS one2012
Role of endothelin in the induction of cardiac hypertrophy in vitro.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- Potential Biomarker and Therapeutic Tools for Pathological Cardiac Hypertrophy and Heart Failure: Extracellular Vesicles.International journal of molecular sciences · 2025Review
- Endothelin-1: Is it Time to "Biomark" the Cardiac-Tumor-Treatment Nexus in Breast Cancer?JACC. CardioOncology · 2023Article
- Could Endothelin-1 Be a Promising Neurohormonal Biomarker in Acute Heart Failure?Diagnostics (Basel, Switzerland) · 2023Review
- The secretome as a biomarker and functional agent in heart failure.The journal of cardiovascular aging · 2023Article
- Robust generation of human-chambered cardiac organoids from pluripotent stem cells for improved modelling of cardiovascular diseases.Stem cell research & therapy · 2022Article
- Data Mining IdentifiesLife (Basel, Switzerland) · 2022Article
- Multi-Omics Characterization of a Human Stem Cell-Based Model of Cardiac Hypertrophy.Life (Basel, Switzerland) · 2022Article
- Maturation of Pluripotent Stem Cell-Derived Cardiomyocytes Enables Modeling of Human Hypertrophic Cardiomyopathy.Stem cell reports · 2021Article
- Differences in Tolerance to Hypoxia: Physiological, Biochemical, and Molecular-Biological Characteristics.Biomedicines · 2020Review
- iPSC-derived progenitor stromal cells provide new insights into aberrant musculoskeletal development and resistance to cancer in down syndrome.Scientific reports · 2020Article
- Article
- Hypertrophy of human embryonic stem cell-derived cardiomyocytes supported by positive feedback between CaPflugers Archiv : European journal of physiology · 2019Article
- Hyperglycemia Enhances Constriction of Retinal Venules via Activation of the Reverse-Mode Sodium-Calcium Exchanger.Diabetes · 2019Article
- The Potential Role of Circulating Endothelial Cells and Endothelial Progenitor Cells in the Prediction of Left Ventricular Hypertrophy in Hypertensive Patients.Frontiers in physiology · 2019Article
- The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes.Frontiers in genetics · 2018Article
- Cardiac-Secreted Factors as Peripheral Metabolic Regulators and Potential Disease Biomarkers.Journal of the American Heart Association · 2016Review
- Article
- Role of Histone Demethylases in Cardiomyocytes Induced to Hypertrophy.BioMed research international · 2016Article
- G-protein Coupled Receptor Signaling in Pluripotent Stem Cell-derived Cardiovascular Cells: Implications for Disease Modeling.Frontiers in cell and developmental biology · 2015Review
- Upregulation of COX-2/PGE2 by ET-1 mediated through Ca2+-dependent signals in mouse brain microvascular endothelial cells.Molecular neurobiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelin (ET-1) is a peptide hormone mediating a wide variety of biological processes and is associated with development of cardiac dysfunction. Generally, ET-1 is regarded as a molecular marker released only in correlation with the observation of a hypertrophic response or in conjunction with other hypertrophic stress. Although the cardiac hypertrophic effect of ET-1 is demonstrated, inotropic properties of cardiac muscle during chronic ET-1-induced hypertrophy remain largely unclear. Through the use of a novel in vitro multicellular culture system, changes in contractile force and kinetics of rabbit cardiac trabeculae in response to 1 nM ET-1 for 24 hours can be observed. Compared to the initial force at t = 0 hours, ET-1 treated muscles showed a ~2.5 fold increase in developed force after 24 hours without any effect on time to peak contraction or time to 90% relaxation. ET-1 increased muscle diameter by 12.5 ± 3.2% from the initial size, due to increased cell width compared to non-ET-1 treated muscles. Using specific signaling antagonists, inhibition of NCX, CaMKII, MAPKK, and IP3 could attenuate the effect of ET-1 on increased developed force. However, among these inhibitions only IP3 receptor blocker could not prevent the increase muscle size by ET-1. Interestingly, though calcineurin-NFAT inhibition could not suppress the effect of ET-1 on force development, it did prevent muscle hypertrophy. These findings suggest that ET-1 provokes both inotropic and hypertrophic activations on myocardium in which both activations share the same signaling pathway through MAPK and CaMKII in associated with NCX activity.
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Registered trials
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.