Sox17 Deficiency Promotes Pulmonary Arterial Hypertension via HGF/c-Met Signaling.

ABSTRACT:

Background

In large-scale genomic studies, Sox17, an endothelial-specific transcription factor, has been suggested as a putative causal gene of pulmonary arterial hypertension (PAH); however, its role and molecular mechanisms remain to be elucidated. We investigated the functional impacts and acting mechanisms of impaired Sox17 (SRY-related HMG-box17) pathway in PAH and explored its potential as a therapeutic target.

Methods

In adult mice, Sox17 deletion in pulmonary endothelial cells (ECs) induced PAH under hypoxia with high penetrance and severity, but not under normoxia.

Results

Key features of PAH, such as hypermuscularization, EC hyperplasia, and inflammation in lung arterioles, right ventricular hypertrophy, and elevated pulmonary arterial pressure

SUBMITTER: Park CS 

PROVIDER: S-EPMC9612711 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature