ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024
Myocardin regulates fibronectin expression and secretion from human pleural mesothelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2024. 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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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- From hPSCs to MSCs: differentiation strategies, pathways, and the emergence of common regulatory networks.Cellular & molecular biology letters · 2026Review
- Quercetin improves ESAT-6-induced pleural mesothelial cell fibrosis by activating the Nrf2/HO-1 pathway.Iranian journal of basic medical sciences · 2026Article
- Research Priorities for Malignant Pleural Organization with Loculation and Failed Drainage.Cells · 2025Review
- Targeting pleuro-alveolar junctions reverses lung fibrosis in mice.Nature communications · 2025Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
During the progression of pleural fibrosis, pleural mesothelial cells (PMCs) undergo a phenotype switching process known as mesothelial-mesenchymal transition (MesoMT). During MesoMT, transformed PMCs become myofibroblasts that produce increased extracellular matrix (ECM) proteins, including collagen and fibronectin (FN1) that is critical to develop fibrosis. Here, we studied the mechanism that regulates FN1 expression in myofibroblasts derived from human pleural mesothelial cells (HPMCs). We found that myocardin (Myocd), a transcriptional coactivator of serum response factor (SRF) and a master regulator of smooth muscle and cardiac muscle differentiation, strongly controls FN1 gene expression. Myocd gene silencing markedly inhibited FN1 expression.
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