SynthesisTranslational research : the journal of laboratory and clinical medicine2022
Differential expression of members of SOX family of transcription factors in failing human hearts.
Synthesis in Translational research : the journal of laboratory and clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 13 citations in OpenAlex.
- A new insight of hypertrophic cardiomyopathy: integrated analysis of differentially expressed genes, expression quantitative trait loci, and mendelian randomization.Journal of cardiothoracic surgery · 2026Article
- Knockdown of SOX4 attenuates sepsis myocardial injury by inhibiting the EZH2/H3K27me3/SOCS3 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- BMDx2: A Tool for Integrating Toxicogenomics-Based Dose-Dependency Analysis and AOP-Based Mechanistic Insights.Small methods · 2025Article
- Epigenetic crossroads in metabolic and cardiovascular health: the role of DNA methylation in type 2 diabetes and cardiovascular diseases.Cardiovascular diabetology · 2025Review
- Identification and Functional Characterization of a NovelChildren (Basel, Switzerland) · 2025Article
- Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.Circulation research · 2025Review
- Sox8: a multifaceted transcription factor in development and disease.Biology open · 2025Review
- A commonly used anti-SOX15 antibody fails to demonstrate specificity in mouse embryos.microPublication biology · 2025Article
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- scGO: interpretable deep neural network for cell status annotation and disease diagnosis.Briefings in bioinformatics · 2024Article
- Identification and Functional Investigation ofDiagnostics (Basel, Switzerland) · 2024Article
- Exploring Health Care Disparities in Genetic Testing and Research for Hereditary Cardiomyopathy: Current State and Future Perspectives.Global medical genetics · 2024Review
- The potential DNA methylation markers of cardiovascular disease in patients with type 2 diabetes.BMC medical genomics · 2023Article
- Linagliptin ameliorated cardiac fibrosis and restored cardiomyocyte structure in diabetic mice associated with the suppression of necroptosis.Journal of diabetes investigation · 2023Article
- Effect of miR-499-5p/SOX6 axis on atrial fibrosis in rats with atrial fibrillation.Open medicine (Warsaw, Poland) · 2023Article
- Novel Genes Involved in Hypertrophic Cardiomyopathy: Data of Transcriptome and Methylome Profiling.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
The Sry-related high-mobility-group box (SOX) gene family, with 20 known transcription factors in humans, plays an essential role during development and disease processes. Several SOX proteins (SOX4, 11, and 9) are required for normal heart morphogenesis. SOX9 was shown to contribute to cardiac fibrosis. However, differential expression of other SOXs and their roles in the failing human myocardium have not been explored. Here, we used the whole-transcriptome sequencing (RNA-seq), gene co-expression, and meta-analysis to examine whether any SOX factors might play a role in the failing human myocardium. RNA-seq analysis was performed for cardiac tissue samples from heart failure (HF) patients due to dilated cardiomyopathy (DCM), or hypertrophic cardiomyopathy (HCM) and healthy donors (NF). The RNA levels of 20 SOX genes from RNA-seq data were extracted and compared to the 3 groups. Four SOX genes whose RNA levels were significantly upregulated in DCM or HCM compared to NF. However, only SOX4 and SOX8 proteins were markedly increased in the HF groups. A moderate to strong correlation was observed between the RNA level of SOX4/8 and fibrotic genes among each individual. Gene co-expression network analysis identified genes associated and respond similarly to perturbations with SOX4 in cardiac tissues. Using a meta-analysis combining epigenetics and genome-wide association data, we reported several genomic variants associated with HF phenotype linked to SOX4 or SOX8. In summary, our results implicate that SOX4 and SOX8 have a role in cardiomyopathy, leading to HF in humans. The molecular mechanism associated with them in HF warrants further investigation.
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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 Socratic graph.