ArticleiScience2025
Depletion of tropomyosin 1.6 alleviates TGF-β1-induced fibroblast activation by promoting the α-SMA-MMP9 matrix-degrading structure.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- DDR1 Modulates Cytoskeletal Remodeling and Podosome Formation in Renal Fibroblasts.International journal of molecular sciences · 2026Article
- Immune Infiltration and Mitochondrial Function in Diabetic Kidney Disease: WGCNA and Machine Learning Identified Hub Genes with Clinical Validation.International journal of molecular sciences · 2026Article
- Splicing isoforms associated with TGFβ-induced myofibroblast activation.BMC molecular and cell biology · 2026Article
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Authors and funding
9 authors.
Funding
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Abstract
Fibroblasts can be transformed into myofibroblasts under pro-fibrotic conditions, which are characterized by increased contractility and reduced matrix degradation. The relationship between contractile activity and matrix degradation is not fully understood. To mimic physiological conditions, fibroblasts were cultured on a collagen gel with low rigidity. We reveal that a tropomyosin isoform, tropomyosin 1.6 (Tpm1.6), plays a pivotal role in the phenotypic switch upon TGF-β1. Tpm1.6 was specifically upregulated by TGF-β1 in renal fibroblasts. Tpm1.6-silencing decreased TGF-β1-induced myofibroblast markers and contractility, and promoted collagen degradation. Remarkably, in Tpm1.6-silenced fibroblasts, TGF-β1 triggered the formation of distinct α-SMA dots enriched with MMP9, promoting collagen degradation. The targeted silencing of Tpm1.6 in activated myofibroblasts by the induction of promoters of
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