Recent evidence shows that increased HIF-1α expression can upregulate the platelet-activating factor receptor (PAFR) on the airway epithelial surface that is increased in smokers and particularly COPD patients.
The role of hypoxia-inducible factor 1 alpha (HIF-1α) in the development and progression of chronic obstructive pulmonary disease (COPD) has also been demonstrated.
The key findings obtained from the present study indicated that high expression of HIF-1α, VEGF and VEGFR2 may be associated with decreased lung function and reduced quality of life, contributing to disease progression in COPD.
The levels of serum hemoglobin, HIF‑1α expression and COPD diagnosis were all identified as independent prognostic variables for the OS and PFS of patients with ccRCC.
It has been shown that deregulation of miRNAs targeting a variety of cellular and molecular pathways such as Notch, Wnt, hypoxia-inducible factor-1α, transforming growth factor, Kras, and Smad could be involved in COPD pathogenesis.
The present study investigated whether sodium tanshinone IIA sulfonate (STS), a water-soluble derivative of tanshinone IIA, can mediate its effect through inhibiting HIF-1α-induced oxidative stress and inflammation in cigarette smoke (CS)-induced COPD in mice.
In addition, when CC-LR mice were bred with transgenic animals that overexpress a constitutively active mutant form of human HIF-1α in the airway epithelium, both COPD- and adenocarcinoma-like phenotypes were observed.