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Regulatory role of NR4A1 in TGF-β signaling in normal, IPF, and estrogen treatment conditions (A) Under normal physiological conditions, brief TGF-β stimulation induces the upregulation of NR4A1. NR4A1 then suppresses epithelial-mesenchymal transition (EMT) and collagen deposition via a negative feedback mechanism. (B) In the IPF state, sustained TGF-β signaling leads to prolonged EMT and collagen deposition, while promoting NR4A1 phosphorylation, which disables its negative feedback regulation of TGF-β signaling. (C) Estrogen treatment enhances NR4A1 <t>transcription</t> and inhibits NR4A1 phosphorylation, thereby restoring its negative feedback regulation on TGF-β signaling.
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Regulatory role of NR4A1 in TGF-β signaling in normal, IPF, and estrogen treatment conditions (A) Under normal physiological conditions, brief TGF-β stimulation induces the upregulation of NR4A1. NR4A1 then suppresses epithelial-mesenchymal transition (EMT) and collagen deposition via a negative feedback mechanism. (B) In the IPF state, sustained TGF-β signaling leads to prolonged EMT and collagen deposition, while promoting NR4A1 phosphorylation, which disables its negative feedback regulation of TGF-β signaling. (C) Estrogen treatment enhances NR4A1 transcription and inhibits NR4A1 phosphorylation, thereby restoring its negative feedback regulation on TGF-β signaling.

Journal: iScience

Article Title: Estrogen upregulates NR4A1 to counter TGF beta induced pulmonary fibrosis therapeutic insights for IPF

doi: 10.1016/j.isci.2026.114756

Figure Lengend Snippet: Regulatory role of NR4A1 in TGF-β signaling in normal, IPF, and estrogen treatment conditions (A) Under normal physiological conditions, brief TGF-β stimulation induces the upregulation of NR4A1. NR4A1 then suppresses epithelial-mesenchymal transition (EMT) and collagen deposition via a negative feedback mechanism. (B) In the IPF state, sustained TGF-β signaling leads to prolonged EMT and collagen deposition, while promoting NR4A1 phosphorylation, which disables its negative feedback regulation of TGF-β signaling. (C) Estrogen treatment enhances NR4A1 transcription and inhibits NR4A1 phosphorylation, thereby restoring its negative feedback regulation on TGF-β signaling.

Article Snippet: RNA was then reverse transcribed into complementary DNA (cDNA) using the GeneCopoeia reverse transcription kit (QP056, USA).

Techniques: Phospho-proteomics