ArticleThe American journal of pathology2004
Smad3 signaling is required for epithelial-mesenchymal transition of lens epithelium after injury.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.
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Who cites it
135 citing papers in PubMed, 284 citations in OpenAlex.
- A Systems View of Posterior Capsule Opacification: TGF-β/ROS Signaling, Mitochondrial Homeostasis, and Injury/Aging Cues-Therapeutic Opportunities.Investigative ophthalmology & visual science · 2026Review
- Impact of the loss of tenascin X on tissue architecture and wound healing of the murine corneal stroma.The ocular surface · 2026Article
- Blockage of SUMO E1 enzyme inhibits ocular lens fibrosis by mediating SMAD4 SUMOylation.Genes & diseases · 2026Article
- Hyperactive PDGFRβ signaling induces cataractogenesis via TGFβ and STAT5-IGF1.Developmental biology · 2025Article
- Distinct transcriptional regulation of the Wnt and TGFβ signaling families associated with wound healing and fibrotic outcomes to lens injury.Experimental eye research · 2025Article
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Identification of a Distal Enhancer That Regulates TGF-β-Induced SNAI1 Expression.Cancer science · 2025Article
- Exosomes containing miR-148a-3p derived from mesenchymal stem cells suppress epithelial-mesenchymal transition in lens epithelial cells.Stem cells translational medicine · 2025Article
- Transcriptome exploration of ferroptosis-related genes in TGFβ- induced lens epithelial to mesenchymal transition during posterior capsular opacification development.BMC genomics · 2024Article
- Analysis of Smad3 in the modulation of stromal extracellular matrix proteins in corneal scarring after alkali injury.Molecular vision · 2024Article
- Understanding the Role of Yes-Associated Protein (YAP) Signaling in the Transformation of Lens Epithelial Cells (EMT) and Fibrosis.Biomolecules · 2023Article
- Lanosterol Synthase Prevents EMT During Lens Epithelial Fibrosis Via Regulating SREBP1.Investigative ophthalmology & visual science · 2023Article
- The SMYD3-MAP3K2 signaling axis promotes tumor aggressiveness and metastasis in prostate cancer.Science advances · 2023Article
- Glycosaminoglycans: Roles in wound healing, formation of corneal constructs and synthetic corneas.The ocular surface · 2023Review
- PRDX1 negatively regulates bleomycin-induced pulmonary fibrosis via inhibiting the epithelial-mesenchymal transition and lung fibroblast proliferation in vitro and in vivo.Cellular & molecular biology letters · 2023Article
- Article
- TGF-β in developmental and fibrogenic EMTs.Seminars in cancer biology · 2022Review
- LncRNA GAS5 regulates migration and epithelial-to-mesenchymal transition in lens epithelial cells via the miR-204-3p/TGFBR1 axis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- HPV-Induced MiR-21 Promotes Epithelial Mesenchymal Transformation and Tumor Progression in Cervical Cancer Cells through the TGFContrast media & molecular imaging · 2022Article
75 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Lens epithelial cells undergo epithelial-mesenchymal transition (EMT) after injury as in cataract extraction, leading to fibrosis of the lens capsule. Fibrosis of the anterior capsule can be modeled in the mouse by capsular injury in the lens, which results in EMT of the lens epithelium and subsequent deposition of extracellular matrix without contamination of other cell types from outside the lens. We have previously shown that signaling via Smad3, a key signal-transducing element downstream of transforming growth factor (TGF)-beta and activin receptors, is activated in lens epithelial cells by 12 hours after injury and that this Smad3 activation is blocked by administration of a TGF-beta 2-neutralizing antibody in mice. We now show that EMT of primary lens epithelial cells in vitro depends on TGF-beta expression and that injury-induced EMT in vivo depends, more specifically, on signaling via Smad3. Loss of Smad3 in mice blocks both morphological changes of lens epithelium to a mesenchymal phenotype and expression of the EMT markers snail, alpha-smooth muscle actin, lumican, and type I collagen in response to injury in vivo or to exposure to exogenous TGF-beta in organ culture. The results suggest that blocking the Smad3 pathway might be beneficial in inhibiting capsular fibrosis after injury and/or surgery.
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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 OpenQuestion graph.