Pathophysiological mechanisms and therapeutic potential of E-selectin in pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a life-threatening pulmonary vascular disease characterized by progressive obstructive remodeling of the small pulmonary arteries. Its pathophysiological core involves perivascular inflammation, endothelial dysfunction, abnormal vascular wall proliferation and in situ thrombosis, arising from interactions between genetic susceptibility and environmental factors. Recent studies have demonstrated the central role of chronic inflammation in the development and progression of PAH. E-selectin, an endothelial-specific adhesion molecule, plays a critical role in mediating the initial adhesion and migration of leukocytes and in triggering the inflammatory cascade. Clinical and experimental studies have demonstrated that E-selectin levels are significantly elevated in both the circulation and local lung tissues of patients with PAH, and that these levels are positively correlated with disease severity. Although observational data have not yet directly established a causal relationship, the combination of its well-recognized proinflammatory properties suggests that E-selectin may function not only as an inflammatory marker but also as a potential key mediator driving pulmonary vascular inflammation and remodeling. This review systematically discusses the biological characteristics of E-selectin and its expression regulation in PAH, further explores the molecular and cellular mechanisms by which it contributes to vascular remodeling, and focuses on potential therapeutic strategies targeting E-selectin, with the aim of providing a new perspective for precision anti-inflammatory treatment in PAH.