ReviewBritish journal of pharmacology2013
The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.
Review in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 90 citations in OpenAlex.
- Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.APL bioengineering · 2026Article
- Article
- Identification of ECE2 signaling in promoting non-small lung cancer progression through ET1/YAP1/MAGEA3 axis.Scientific reports · 2025Article
- Insulin-like growth factor 1 (IGF-1)-induced changes in cardiac inducible nitric oxide synthase (iNOS) in obese rats.Frontiers in endocrinology · 2025Article
- Vascularization of PEGylated fibrin hydrogels increases the proliferation of human iPSC-cardiomyocytes.Journal of biomedical materials research. Part A · 2024Article
- Effect of Cold Adaptation on the State of Cardiovascular System and Cardiac Tolerance to Ischemia/Reperfusion Injury.Iranian biomedical journal · 2024Review
- Blood vessels in a dish: the evolution, challenges, and potential of vascularized tissues and organoids.Frontiers in cardiovascular medicine · 2024Review
- Cardiac optogenetics: shining light on signaling pathways.Pflugers Archiv : European journal of physiology · 2023Review
- Extracellular vesicle-derived CircWhsc1 promotes cardiomyocyte proliferation and heart repair by activating TRIM59/STAT3/Cyclin B2 pathway.Journal of advanced research · 2023Article
- Could Endothelin-1 Be a Promising Neurohormonal Biomarker in Acute Heart Failure?Diagnostics (Basel, Switzerland) · 2023Review
- Review
- When natural antibodies become pathogenic: autoantibodies targeted against G protein-coupled receptors in the pathogenesis of systemic sclerosis.Frontiers in immunology · 2023Review
- Multi-Omics Characterization of a Human Stem Cell-Based Model of Cardiac Hypertrophy.Life (Basel, Switzerland) · 2022Article
- Article
- The vasculature: a therapeutic target in heart failure?Cardiovascular research · 2022Review
- The Causal Relationship between Endothelin-1 and Hypertension: Focusing on Endothelial Dysfunction, Arterial Stiffness, Vascular Remodeling, and Blood Pressure Regulation.Life (Basel, Switzerland) · 2021Review
- Engineered models of the human heart: Directions and challenges.Stem cell reports · 2021Review
- Nucleoplasmic CaCirculation research · 2021Article
- Secondary Metabolites of Plants as Modulators of Endothelium Functions.International journal of molecular sciences · 2021Review
- Autocrine Signaling in Cardiac Remodeling: A Rich Source of Therapeutic Targets.Journal of the American Heart Association · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledEndothelin-1 (ET-1) is a critical autocrine and paracrine regulator of cardiac physiology and pathology. Produced locally within the myocardium in response to diverse mechanical and neurohormonal stimuli, ET-1 acutely modulates cardiac contractility. During pathological cardiovascular conditions such as ischaemia, left ventricular hypertrophy and heart failure, myocyte expression and activity of the entire ET-1 system is enhanced, allowing the peptide to both initiate and maintain maladaptive cellular responses. Both the acute and chronic effects of ET-1 are dependent on the activation of intracellular signalling pathways, regulated by the inositol-trisphosphate and diacylglycerol produced upon activation of the ET(A) receptor. Subsequent stimulation of protein kinases C and D, calmodulin-dependent kinase II, calcineurin and MAPKs modifies the systolic calcium transient, myofibril function and the activity of transcription factors that coordinate cellular remodelling. The precise nature of the cellular response to ET-1 is governed by the timing, localization and context of such signals, allowing the peptide to regulate both cardiomyocyte physiology and instigate disease. LINKED ARTICLES: This article is part of a themed section on Endothelin. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2013.168.issue-1.
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Identifiers
What Socratic holds
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 Socratic graph.