Fig. 9: FOXN3 demonstrates a significant correlation with the progression of clinical lung fibrosis.
From: Phosphorylation of FOXN3 by NEK6 promotes pulmonary fibrosis through Smad signaling
a–c Histological immunohistochemical staining analysis was performed to assess the expression levels of FOXN3 (b) and Smad4 (c) in fibrotic lesion areas and corresponding adjacent normal areas of one patient diagnosed with lung fibrosis, with scale bars set at 100 μm. Trichrome staining was carried out simultaneously to confirm the presence of the fibrotic lesions (a), with scale bars set at 100 μm. A representative image (a) was taken from at least three different areas for each sample. d Quantitative analysis of b and c was shown by immunoreactive score (IRS) (n = 20). e A proposed working model clarifies the activation of Smad signaling in response to pro-fibrotic stimuli. The schematic representation was created in BioRender. LIAN, J. (2024) https://BioRender.com/d99u033. The data (d) was assessed by a two-tailed Student’s t test and is shown as the mean ± SD.
