ArticleJournal of cellular and molecular medicine2021
PU.1 inhibition attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II by reducing TGF-β1/Smads pathway activation.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer.Cell death & disease · 2025Article
- Interaction between nuclear-translocated cellular communication network factor 2 and purine-rich box 1 regulates the expression of fibrosis-related genes.Journal of cell communication and signaling · 2025Article
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025Review
- Epigallocatechin gallate regulates the myeloid-specific transcription factor PU.1 in macrophages.PloS one · 2024Article
- CD4+ T-cell subsets in autoimmune hepatitis: A review.Hepatology communications · 2023Review
- [mRNA Expression Profile Changes in Angiotensin-Ⅱ-Induced Atrial Myocardial Fibrosis in Rats].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- ANGPTL8 accelerates liver fibrosis mediated by HFD-induced inflammatory activity via LILRB2/ERK signaling pathways.Journal of advanced research · 2023Article
- PU.1 inhibition does not attenuate cardiac function deterioration or fibrosis in a murine model of myocardial infarction.Molecular and cellular biochemistry · 2023Article
- Article
- PU.1 inhibition attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II by reducing TGF-β1/Smads pathway activation.Journal of cellular and molecular medicine · 2021Article
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14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis serves a critical role in driving atrial remodelling-mediated atrial fibrillation (AF). Abnormal levels of the transcription factor PU.1, a key regulator of fibrosis, are associated with cardiac injury and dysfunction following acute viral myocarditis. However, the role of PU.1 in atrial fibrosis and vulnerability to AF remain unclear. Here, an in vivo atrial fibrosis model was developed by the continuous infusion of C57 mice with subcutaneous Ang-II, while the in vitro model comprised atrial fibroblasts that were isolated and cultured. The expression of PU.1 was significantly up-regulated in the Ang-II-induced group compared with the sham/control group in vivo and in vitro. Moreover, protein expression along the TGF-β1/Smads pathway and the proliferation and differentiation of atrial fibroblasts induced by Ang-II were significantly higher in the Ang-II-induced group than in the sham/control group. These effects were attenuated by exposure to DB1976, a PU.1 inhibitor, both in vivo and in vitro. Importantly, in vitro treatment with small interfering RNA against Smad3 (key protein of TGF-β1/Smads signalling pathway) diminished these Ang-II-mediated effects, and the si-Smad3-mediated effects were, in turn, antagonized by the addition of a PU.1-overexpression adenoviral vector. Finally, PU.1 inhibition reduced the atrial fibrosis induced by Ang-II and attenuated vulnerability to AF, at least in part through the TGF-β1/Smads pathway. Overall, the study implicates PU.1 as a potential therapeutic target to inhibit Ang-II-induced atrial fibrosis and vulnerability to AF.
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