Role of HMGB1 in the formation of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism.

Abstract

Acute pulmonary embolism (PE) may be a common but fatal condition in several countries; in untreated or inadequately therapeutic PE patients, is a commonly occurring long-term complication affecting patient survival treatment and prognosis, contributing to right heart disease and may even be fatal. To date, the pathogenesis of chronic thromboembolic pulmonary hypertension (CTEPH) due to acute pulmonary embolism remains unclear; hence, there is an immediate demand for medications that are directly aimed at both preventing and managing the progression of CTEPH. Previous studies have shown that the inflammatory response is associated with thrombosis and the development of pulmonary cardiovascular disease. High-mobility Group B 1 (HMGB1), a damage-associated molecular pattern (DAMP), is involved in deep vein thrombosis and inflammatory reactions, vascular remodeling, and thrombosis in pulmonary hypertension. Therefore, we hypothesized that HMGB1 participates in the process of CTEPH development after acute PE. This paper details the dynamic changes in HMGB1 and the relationship between HMGB1 and the advancement of CTEPH after acute PE to better understand the pathogenic mechanisms and potential clinical applications.