ArticleScientific reports2018
sox9b is required in cardiomyocytes for cardiac morphogenesis and function.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- AOP Report: Aryl Hydrocarbon Receptor Activation Leads to Early-Life Stage Mortality via Sox9 Repression-Induced Craniofacial and Cardiac Malformations.Environmental toxicology and chemistry · 2023Pooled it
- Association Between Environmental Chemicals Phthalates and Stroke Among the US Adults: A Cross-Sectional Study.Cardiovascular toxicology · 2026Article
- Article
- Nomilin Reversed Cardiotoxicity Caused by Co-exposure to Zearalenone and Deoxynivalenol via the Keap1/Nrf2 Signaling Pathway in Zebrafish.Plant foods for human nutrition (Dordrecht, Netherlands) · 2024Article
- Adverse Effect of Metallic Gold and Silver Nanoparticles onNanomaterials (Basel, Switzerland) · 2023Article
- Linagliptin ameliorated cardiac fibrosis and restored cardiomyocyte structure in diabetic mice associated with the suppression of necroptosis.Journal of diabetes investigation · 2023Article
- Trajectory reconstruction identifies dysregulation of perinatal maturation programs in pluripotent stem cell-derived cardiomyocytes.Cell reports · 2023Article
- Methyl Parathion Exposure Induces Development Toxicity and Cardiotoxicity in Zebrafish Embryos.Toxics · 2023Article
- Melatonin Prevents NaAsOAntioxidants (Basel, Switzerland) · 2022Article
- Identification of a novel heterozygous SOX9 variant in a Chinese family with congenital heart disease.Molecular genetics & genomic medicine · 2022Article
- Article
- Embryonic ethanol exposure alters expression of sox2 and other early transcripts in zebrafish, producing gastrulation defects.Scientific reports · 2020Article
- On Zebrafish Disease Models and Matters of the Heart.Biomedicines · 2019Review
- Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019Review
- Differential Hepatic Gene Expression Profile of Male Fathead Minnows Exposed to Daily Varying Dose of Environmental Contaminants Individually and in Mixture.Frontiers in endocrinology · 2018Article
- Translational Toxicology in Zebrafish.Current opinion in toxicologyArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The high mobility group transcription factor SOX9 is expressed in stem cells, progenitor cells, and differentiated cell-types in developing and mature organs. Exposure to a variety of toxicants including dioxin, di(2-ethylhexyl) phthalate, 6:2 chlorinated polyfluorinated ether sulfonate, and chlorpyrifos results in the downregulation of tetrapod Sox9 and/or zebrafish sox9b. Disruption of Sox9/sox9b function through environmental exposures or genetic mutations produce a wide range of phenotypes and adversely affect organ development and health. We generated a dominant-negative sox9b (dnsox9b) to inhibit sox9b target gene expression and used the Gal4/UAS system to drive dnsox9b specifically in cardiomyocytes. Cardiomyocyte-specific inhibition of sox9b function resulted in a decrease in ventricular cardiomyocytes, an increase in atrial cardiomyocytes, hypoplastic endothelial cushions, and impaired epicardial development, ultimately culminating in heart failure. Cardiomyocyte-specific dnsox9b expression significantly reduced end diastolic volume, which corresponded with a decrease in stroke volume, ejection fraction, and cardiac output. Further analysis of isolated cardiac tissue by RT-qPCR revealed cardiomyocyte-specific inhibition of sox9b function significantly decreased the expression of the critical cardiac development genes nkx2.5, nkx2.7, and myl7, as well as c-fos, an immediate early gene necessary for cardiomyocyte progenitor differentiation. Together our studies indicate sox9b transcriptional regulation is necessary for cardiomyocyte development and function.
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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.