ArticleFrontiers in physiology2021
Cell Type Dependent Suppression of Inflammatory Mediators by Myocardin Related Transcription Factors.
Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Pro-inflammatory LPS drives production and release of the chemokine MCP-1 in human coronary artery smooth muscle cells.Molecular and cellular biochemistry · 2026Article
- Suppression of smooth muscle cell inflammation by myocardin-related transcription factors involves inactivation of TANK-binding kinase 1.Scientific reports · 2024Article
- SRF Rearrangements in Soft Tissue Tumors with Muscle Differentiation.Biomolecules · 2022Article
- BAF60c prevents abdominal aortic aneurysm formation through epigenetic control of vascular smooth muscle cell homeostasis.The Journal of clinical investigation · 2022Article
- Exploring the mechanism of Shexiang Tongxin dropping pill in the treatment of microvascular angina through network pharmacology and molecular docking.Annals of translational medicine · 2022Article
- Identification of microRNA-mRNA-TF regulatory networks in periodontitis by bioinformatics analysis.BMC oral health · 2022Article
- MRTF may be the missing link in a multiscale mechanobiology approach toward macrophage dysfunction in space.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardin related transcription factors (MRTFs: MYOCD/myocardin, MRTF-A, and MRTF-B) play a key role in smooth muscle cell differentiation by activating contractile genes. In atherosclerosis, MRTF levels change, and most notable is a fall of MYOCD. Previous work described anti-inflammatory properties of MRTF-A and MYOCD, occurring through RelA binding, suggesting that MYOCD reduction could contribute to vascular inflammation. Recent studies have muddled this picture showing that MRTFs may show both anti- and pro-inflammatory properties, but the basis of these discrepancies remain unclear. Moreover, the impact of MRTFs on inflammatory signaling pathways in tissues relevant to human arterial disease is uncertain. The current work aimed to address these issues. RNA-sequencing after forced expression of myocardin in human coronary artery smooth muscle cells (hCASMCs) showed reduction of pro-inflammatory transcripts, including
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