Pulmonary hypertension (PH) is a progressive vascular disease, yet the underlying cell-type-specific molecular networks and diagnostic biomarkers remain incompletely defined. Integrating single-cell and bulk transcriptomics, we identified 14 pulmonary cell types in PH, with smooth muscle cells (SMCs) as a central communication hub interacting with monocytes and macrophages. High-dimensional weighted gene co-expression network analysis (hdWGCNA) revealed 4 SMC modules enriched in extracellular matrix organization, TGF-β, and HIF-1 pathways. A five-gene diagnostic signature distinguished PH from controls with an area under the curve of 0.895. Immune infiltration and enrichment analysis showed that activated CD4 memory T cells, activated dendritic cells, and resting mast cells increased in the PH group, while angiogenesis and epithelial-mesenchymal transition pathway were upregulated. In hypoxic human pulmonary artery SMCs, milk fat globule-epidermal growth factor-8 (MFGE8), secreted frizzled-related protein 2 (SFRP2), S100 calcium-binding protein A11 (S100A11), and procollagen C-endopeptidase enhancer 2 (PCOLCE2) were upregulated, and their knockdown suppressed proliferation, highlighting them as potential biomarkers and drivers of vascular remodeling, revealing a new molecular mechanism for PH and providing insights for potential therapeutic targets.
No takes yet. Share an insight, caveat, or question.
Wu et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: