BMP9 Modulates IL-33 Signaling to Mitigate EndMT in Pulmonary Arterial Hypertension.

ABSTRACT:

Background

Pulmonary arterial hypertension (PAH) is a progressive disorder involving disrupted BMP (bone morphogenetic protein) signaling, pulmonary inflammation, and endothelial-to-mesenchymal transition (EndMT). We hypothesized that IL (interleukin)-33 signaling contributes to PAH progression by inducing EndMT and interacting with BMP9, a key modulator of inflammation and vascular remodeling.

Methods

IL-33 expression was assessed in lung tissues from Sugen/hypoxia and control mice, as well as in pulmonary arterial endothelial cells (PAECs) and lung tissues from patients with PAH and healthy donors. EndMT and signaling pathways were analyzed in PAECs and microvascular endothelial cells (MVECs) exposed to IL-33, BMP9, and sST2 (soluble supression of tumorigenicity 2) using q

SUBMITTER: Becher C 

PROVIDER: S-EPMC12822782 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature