This study demonstrates the down-regulator of HMGB1, EP, as a potential therapeutic agent for pulmonary fibrosis, as assessed by a non-invasive HPXe MRI protocol.
In bleomycin-induced pulmonary fibrosis in mice, HMGB1 protein was predominantly up-regulated in bronchiolar epithelial cells at early phase and in alveolar epithelial and inflammatory cells in fibrotic lesions at later phase.
Bleomycin (BLM)-induced PF in Nrf2-knockout (Nrf2<sup>-/-</sup> ) and wild-type (WT) mice and transforming growth factor β1 (TGF-β1)-induced EMT in rat type II alveolar epithelial cell line (RLE-6TN) and human alveolar epithelial cell line (A549) were established to observe the relationship among Nrf2, HMGB1, and EMT by western blot and immunohistochemistry.
Therefore, the present study aimed to examine the potential molecular mechanisms that underlie HMGB1‑induced lung fibrosis via the regulation of NF‑κB and TGF‑β1.
An abnormal high mobility group box 1 (HMGB1) activation and a decrease in receptor for advanced glycation end-product (RAGE) play a key role in the pathogenesis of pulmonary fibrosis.
This study investigated the roles of HMGB1 and thrombin in the pathophysiology of bleomycin-induced pulmonary fibrosis and the efficacy of recombinant human soluble thrombomodulin (rhTM).
Higher levels of HMGB1 were associated with earlier onset of AE in stable IPF patients and with shorter survival in AE-IPF patients (P = 0.030 and 0.001, respectively).