Hyperglycaemia-induced fibrotic and inflammatory gene expression alterations in lung epithelial cells: Implications for pulmonary fibrosis development.

Hyperglycaemia has a significant long-term impact on multiple organ systems, including renal, cardiovascular, central nervous, hepatic and ocular systems, leading to the gradual loss of their functional abilities. Numerous studies have elucidated the pathophysiology, etiology, and consequences of hyperglycaemia on these organs. The pulmonary system is also considered as a target of hyperglycaemia, several factors cause lung injury which leads to the development of pulmonary fibrosis, a chronic fibrotic disease with usual interstitial pneumonia patterns. Nevertheless, the effects of hyperglycaemia on the development of pulmonary fibrosis remain poorly understood. We intend to understand the cellular and morphological changes, and the progression of fibrosis in lung epithelial cells subjected to hyperglycaemia. Our experimental data indicate that hyperglycaemia induces fibrotic and inflammatory alterations in cultured lung epithelial cells. These alterations are facilitated by the upregulation of genes related to fibrosis and inflammation, promoting cell proliferation and migration. Further research is required to comprehensively elucidate the impact of hyperglycaemia during lung injury progression of fibrosis, these findings may reveal novel mechanisms that may help in the assessment and treatment of lung ailments in people with hyperglycaemia.