ArticleJournal of cellular and molecular medicine2019
FOXC1 up-regulates the expression of toll-like receptors in myocardial ischaemia.
Article in Journal of cellular and molecular medicine, 2019. 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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- A Meta-Analysis Approach to Gene Regulatory Network Inference Identifies Key Regulators of Cardiovascular Diseases.International journal of molecular sciences · 2024Pooled it
- Exploring the causal relationship and pathogenesis of intracranial aneurysms with osteoporosis based on Mendelian randomization and bioinformatics study.Journal of bone and mineral metabolism · 2026Article
- Integrated multi-omics profiling of the early post-infarct heart reveals a hub gene network associated with myeloid-driven inflammation.Frontiers in cardiovascular medicine · 2026Article
- Shared Genetic Characteristics of Coronary Artery Disease and Peripheral artery Disease: Insights From Integrated Bioinformatics Analysis of RNA-Sequencing Data.Bioinformatics and biology insights · 2025Article
- Bioinformatics analysis of the expression of potential common genes and immune-related genes between atrial fibrillation and chronic kidney disease.Frontiers in cardiovascular medicine · 2025Article
- Proximal telomeric decompaction due to telomere shortening drives FOXC1-dependent myocardial senescence.Nucleic acids research · 2024Article
- CKLF1, transcriptionally activated by FOXC1, promotes hypoxia/reoxygenation‑induced oxidative stress and inflammation in H9c2 cells by NLRP3 inflammasome activation.Experimental and therapeutic medicine · 2024Article
- Review
- Proteomic analysis reveals changes in the proteome of human THP-1 macrophages infected withFrontiers in cellular and infection microbiology · 2023Article
- Identification of common molecular signatures of SARS-CoV-2 infection and its influence on acute kidney injury and chronic kidney disease.Frontiers in immunology · 2023Article
- Potential therapeutic strategies for myocardial infarction: the role of Toll-like receptors.Immunologic research · 2022Review
- Clinical Significance of MAP-7 and FOXC1 in Egyptian Acute Myeloid Leukemia Patients.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Overexpression of Foxc1 ameliorates sepsis‑associated encephalopathy by inhibiting microglial migration and neuroinflammation through the IκBα/NF‑κB pathway.Molecular medicine reports · 2022Article
- Regulatory mechanism of fibrosis-related genes in patients with heart failure.Frontiers in genetics · 2022Article
- Targeting the forkhead box protein P1 pathway as a novel therapeutic approach for cardiovascular diseases.Heart failure reviews · 2022Review
- FOXC1 up-regulates the expression of toll-like receptors in myocardial ischaemia.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
11 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischaemia (MI) remains a major cause of death and disability worldwide. Accumulating evidence suggests a significant role for innate immunity, in which the family of toll-like receptors (TLRs) acts as an essential player. We previously reported and reviewed the changes of Tlr expression in models of MI. However, the underlying mechanisms regulating Tlr expression in MI remain unclear. The present study first screened transcription factors (TFs) that potentially regulate Tlr gene transcription based on in silico analyses followed by experimental verification, using both in vivo and in vitro models. Forkhead box C1 (FOXC1) was identified as a putative TF, which was highly responsive to MI. Next, by focusing on two representative TLR subtypes, an intracellular subtype TLR3 and a cell-surface subtype TLR4, the regulation of FOXC1 on Tlr expression was investigated. The overexpression or knockdown of FoxC1 was observed to up- or down-regulate Tlr3/4 mRNA and protein levels, respectively. A dual-luciferase assay showed that FOXC1 trans-activated Tlr3/4 promoter, and a ChIP assay showed direct binding of FOXC1 to Tlr3/4 promoter. Last, a functional study of FOXC1 was performed, which revealed the pro-inflammatory effects of FOXC1 and its destructive effects on infarct size and heart function in a mouse model of MI. The present study for the first time identified FOXC1 as a novel regulator of Tlr expression and described its function in MI.
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