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Snhg18 promotes hypoxic pulmonary hypertension by enhancing glycolysis

GSE305837 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/05/01 Platform GPL24247
Summary
Pulmonary hypertension (PH) is a life-threatening vascular disorder characterized by progressive pulmonary vascular remodeling. In this study, we aim to clarify the lncRNA small nucleolar RNA host gene 18 (Snhg18) implicated in pulmonary vascular remodeling and investigate its underlying mechanisms. Snhg18 is upregulated in pulmonary artery smooth muscle cells (PASMCs) and lung tissues under hypoxic conditions. Inhibition of Snhg18 attenuates cell proliferation in vitro and in vivo. Snhg18 interacts with the m6A “reader” protein heterogeneous nuclear ribonucleoprotein A2/B1 (Hnrnpa2b1), thus increasing enolase 3 (Eno3) mRNA stability in an m6A-dependent manner. The elevation of Eno3 augments glycolysis of PASMCs, thus promoting cell proliferation and vascular remodeling. Our study demonstrates the important role of Snhg18/Hnrnpa2b1/Eno3 axis in pulmonary vascular remodeling, and provide a potential novel therapeutic target for PH.
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Also filed as BioProject PRJNA1307994 and SRA study SRP609846. Searching any of these in the dataset finder brings you back here.

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