The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke‐induced inflammation in chronic obstructive pulmonary disease

Abstract

Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease with irreversible and continuous progression. It has become the fifth most burdensome disease and the third most deadly disease globally. Therefore, the prevention and treatment of COPD are urgent, and it is also important to clarify the pathogenesis of it. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) can cause lung inflammation and other pathological mechanisms in the airways and lung tissue. Airway inflammation is one of the important mechanisms leading to the pathogenesis of COPD. Recent studies have shown that high mobility group box 1 (HMGB1) is involved in the occurrence and development of respiratory diseases, including COPD. HMGB1 is a typical damage‐associated molecular pattern (DAMP) protein, which mainly exerts its activity by binding to the receptor for advanced glycation end products (RAGE) and toll‐like receptor 4 (TLR4) and further participate in the process of airway inflammation. Studies have shown that the abnormal expression of HMGB1, RAGE, and TLR4 are related to inflammation in COPD. Herein, we discuss the roles of HMGB1, RAGE, and TLR4 in CS/cigarette smoke extract‐induced inflammation in COPD, providing a new target for the diagnosis, treatment and prevention of COPD.

Combined analysis of bulk RNA and single-cell RNA sequencing to identify pyroptosis-related markers and the role of dendritic cells in chronic obstructive pulmonary disease

“…HMGB1 also appears to regulate the adhesion and migration of neutrophils, similar to AGER/RAGE and ITGAM. Studies have confirmed that HMGB1 is involved in airway inflammatory processes and that its aberrant expression is associated with inflammation in COPD [ 30 ]. NLRP3 is associated with neutrophil migration and promotes interleukin-18 (IL-18) production.…”

Identification of related-genes of T cells in lung tissue of chronic obstructive pulmonary disease based on bioinformatics and experimental validation

“…TLR9 expression is increasedin the airway epithelial cells of COPD patients, and more inflammatoryfactors, such as IL-6 and CXCL5, are secreted to affect lung function 57 . Cigarette smoke may mediated COPD lung inflammation through the HMGB1/RAGE/TLR4 signaling pathway 58 . As a classic inflammatory signaling pathway, MAPK alsoplays an important role in COPD 59 , 60 .…”

Advanced Biomarkers of Hepatotoxicity in Psychiatry: A Narrative Review and Recommendations for New Psychoactive Substances

“…The first relates to COPD, which is triggered by cigarette smoking, and the role of the HMGB1/RAGE/TLR4 signalling pathway in this process. Cigarette smoke can cause lung inflammation, and HMGB1 and its receptors are involved in the activation of airway inflammation, which in chronic exposure is very likely to lead to the development of COPD [172]. The second also deals with COPD, for which cigarette smoke exposure is a factor in its development, but focuses only on the role of the RAGE receptor and its ligand HMGB1.…”