ArticleJCI insight2022
Sine oculis homeobox homolog 1 plays a critical role in pulmonary fibrosis.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Murine models of pulmonary fibrosis: mechanisms, limitations and translational insights.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Article
- Adipocyte-specific deletion of sine oculis homeobox homolog 1 inhibits lipolysis and reduces skin fibrosis.JCI insight · 2026Article
- LncRNA IGF2-AS serves as a miR-106b-5p sponge to induce apoptosis and inflammatory reaction of bronchial epithelial cells in COPD.BMC pulmonary medicine · 2025Article
- Macrophage migration inhibitory factor mediates joint capsule fibrosis via facilitating phospholipid metabolite PGE2 production in fibroblasts.Cellular and molecular life sciences : CMLS · 2025Article
- The multifaced role of the macrophage migration inhibitory factor family in organ fibrosis.American journal of physiology. Cell physiology · 2025Review
- Novel AT2 Cell Subpopulations and Diagnostic Biomarkers in IPF: Integrating Machine Learning with Single-Cell Analysis.International journal of molecular sciences · 2024Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
Corrections and comments
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Authors and funding
20 authors at 9 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal disease with limited treatment options. The role of the developmental transcription factor Sine oculis homeobox homolog 1 (SIX1) in the pathophysiology of lung fibrosis is not known. IPF lung tissue samples and IPF-derived alveolar type II cells (AT2) showed a significant increase in SIX1 mRNA and protein levels, and the SIX1 transcriptional coactivators EYA1 and EYA2 were elevated. Six1 was also upregulated in bleomycin-treated (BLM-treated) mice and in a model of spontaneous lung fibrosis driven by deletion of Telomeric Repeat Binding Factor 1 (Trf1) in AT2 cells. Conditional deletion of Six1 in AT2 cells prevented or halted BLM-induced lung fibrosis, as measured by a significant reduction in histological burden of fibrosis, reduced fibrotic mediator expression, and improved lung function. These effects were associated with increased macrophage migration inhibitory factor (MIF) in lung epithelial cells in vivo following SIX1 overexpression in BLM-induced fibrosis. A MIF promoter-driven luciferase assay demonstrated direct binding of Six1 to the 5'-TCAGG-3' consensus sequence of the MIF promoter, identifying a likely mechanism of SIX1-driven MIF expression in the pathogenesis of lung fibrosis and providing a potentially novel pathway for targeting in IPF therapy.
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Registered trials
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.