ArticleCellular and molecular life sciences : CMLS2025
Rab26 promotes hypoxia-induced hyperproliferation of PASMCs by modulating the AT1R-STAT3-YAP axis.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Shortened Pulmonary Pulse Wave Transit Time in High-Altitude Residents Without Pulmonary Hypertension: An Doppler Echocardiography Study.Physiological research · 2026Article
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14 authors.
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Abstract
The hyper-proliferation of pulmonary artery smooth muscle cells (PASMCs) significantly contributes to pulmonary vascular remodeling (PVR) in chronic hypoxic pulmonary arterial hypertension (PAH), leading to right ventricular dysfunction and increased mortality. Despite the critical role of this process, the mechanisms underlying hypoxia-induced PASMCs hyper-proliferation remain largely unexplored. In this study, hypoxia was found to upregulate Rab26 expression in rat PASMCs (rPASMCs) and lung tissue in a PAH mouse model. Silencing Rab26 reduced rPASMCs hyper-proliferation. Rab26 interacted with angiotensin II Type 1 receptor (AT1R) and modulated its transport to the cell surface, thereby activating Signal Transducer and Activator of Transcription 3 (STAT3), upregulating Yes-associated protein 1 (YAP1) expression, and promoting YAP1 nuclear translocation. Moreover, hypoxia enhanced the interaction between YAP and STAT3, with STAT3 also facilitating YAP nuclear translocation. Rab26 deficiency downregulates the levels of pSTAT3 and YAP1 in lung tissue and smooth muscle arteries and attenuated the hypoxia-induced PVR. Rab26 deficiency results in decreased expression of pSTAT3 and YAP1 in lung tissue and pulmonary smooth muscle arteries, while also attenuating hypoxia-induced PVR. Furthermore, pharmacological inhibition of AT1R and pSTAT3 further reduces pSTAT3 and YAP1 expression both in wild-type (WT) and Rab26
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