Key result
Endothelial cell heterogeneity drives vascular remodeling in pulmonary hypertension.
Understanding the heterogeneity of pulmonary endothelial cells through single-cell RNA sequencing provides critical insights into the pathogenesis of pulmonary hypertension and identifies novel therapeutic opportunities.
The lung endothelium is essential for maintaining normal lung structure and plays a key role in gas exchange, barrier function, angiogenesis, vascular tone, and inflammation regulation. The advent of single-cell RNA sequencing has revealed the unique heterogeneity of pulmonary endothelial cells (ECs) in their function, morphology, and localization. Pulmonary hypertension (PH) is a progressive vascular disorder marked by elevated pulmonary arterial pressure and vascular remodeling. Central to its pathogenesis is EC dysfunction, and emerging evidence highlights EC heterogeneity in driving the complexity of PH. The distinct lung endothelial subpopulations exhibit diverse molecular signatures and functional responses under PH. A complete picture of how these different subpopulations contribute to vascular remodeling of PH is critical to identify novel therapeutic opportunities. This brief review summarizes recent insights into EC dysfunction in PH, focusing on the role of specialized EC subsets and novel therapeutic strategies targeting EC dysfunction. We highlight the integration of cutting-edge technologies in understanding how endothelial heterogeneity shapes the trajectory of PH and opens new avenues for future therapeutic innovations.
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Zhao et al. (2025) conducted a review in Pulmonary hypertension. Endothelial cell heterogeneity was evaluated. Recent insights highlight the role of specialized endothelial cell subsets and heterogeneity in driving the pathogenesis and vascular remodeling of pulmonary hypertension.
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