The role and mechanism of TNALP in granulation tissue proliferation and fibrosis after tracheal injury.

Tracheal injury repair involves the formation of granulation tissue and eventual fibrosis. This process is often initiated by various damaging factors such as tracheobronchial tuberculosis and tracheal intubation. These factors can disrupt the normal repair mechanisms of the trachea, leading to hyperplasia of granulation tissue and scar formation. Over time, this abnormal repair process can progress to tracheal fibrosis, which significantly impacts patients' quality of life and safety. The complexity of the disease, along with its large patient base, highlights the urgent need for effective treatment methods.TNALP, an enzyme involved in tissue repair, has emerged as a critical target for fibrosis treatment in various organs. However, its specific role in tracheal injury repair remains unclear. Our research aims to address this gap by investigating TNALP expression in patients with tracheal injury. We found that TNALP is upregulated in these patients. Additionally, experiments conducted on rat models showed that reducing TNALP levels can effectively inhibit the proliferation of granulation tissue in the trachea and improve the degree of tracheal fibrosis. Conversely, overexpression of TNALP exacerbates airway fibrosis post-injury. To further elucidate the role of TNALP in tracheal injury repair, our study utilizes patients with tracheal granulation tissue hyperplasia, SD rat tracheal granulation hyperplasia models, and tracheal fibroblasts. By constructing both in vivo and in vitro tracheal injury repair models, we aim to explore the mechanisms underlying TNALP-mediated repair processes in the trachea.