ArticleCurrent topics in medicinal chemistry2017
Proteomic Analysis of Endothelin-1 Targets in the Regulation of Cardiomyocyte Proliferation.
Article in Current topics in medicinal chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Endothelin-1 Stimulates the Growth of Visceral and Subcutaneous Human Preadipocytes through Similar and Alternative Signaling Pathways via Type A and Type B Endothelin Receptors: Potential Implications for Therapeutic Strategies for Obesity and Metabolic Disorders.International journal of medical sciences · 2025Article
- Epigenetic regulation of embryonic ectoderm development in stem cell differentiation and transformation during ontogenesis.Cell proliferation · 2023Review
- Review
- Plasma endothelin-1 levels are increased in atrial fibrillation patients with hyperthyroidism.PloS one · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Hypoxia is a fetal stressor that leads to the production of endothelin-1 (ET-1). Previous work has shown that ET-1 treatment leads to the premature terminal differentiation of fetal cardiomyocytes. However, the precise mechanism is unknown. We tested the hypothesis that the fetal cardiomyocyte proteome will be greatly altered due to ET-1-treatment, which reveals a potential molecular mechanism of ET-1-induced terminal differentiation. Over a thousand proteins were detected in the fetal cardiomyocytes and among them 75 proteins were significantly altered due to ET-1 treatment. Using IPA pathway analysis, the merged network depicted several key proteins that appeared to be involved in regulating proliferation, including: EED, UBC, ERK1/2, MAPK, Akt, and EGFR. EED protein, which is associated with regulating proliferation via epigenetic mechanisms, is of particular interest. Herein we propose a model of the molecular mechanism by which ET-1 induced cardiomyocyte terminal differentiation occurs.
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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.