ArticleMolecular medicine reports2022
LncRNA GAS5 promotes spermidine‑induced autophagy through the miRNA‑31‑5p/NAT8L axis in pulmonary artery endothelial cells of patients with CTEPH.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- LncRNA APF suppresses pulmonary vascular remodeling in chronic thromboembolic pulmonary hypertension through the miR-188-3p/ATG7-mediated autophagy pathway.American journal of translational research · 2026Article
- miRNAs in Pulmonary Hypertension: Mechanistic Insights and Therapeutic Potential.Biomedicines · 2025Review
- Emerging connectivity of programmed cell death pathways and pulmonary vascular remodelling during pulmonary hypertension.Journal of cellular and molecular medicine · 2024Review
- Fetal hypoplastic lungs have multilineage inflammation that is reversed by amniotic fluid stem cell extracellular vesicle treatment.Science advances · 2024Article
- Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024Review
- Emerging Epigenetic Targets and Their Molecular Impact on Vascular Remodeling in Pulmonary Hypertension.Cells · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Chronic thromboembolic pulmonary hypertension (CTEPH) is a leading cause of pulmonary hypertension. The present study investigated the mechanisms of long non‑coding RNA growth arrest‑specific transcript 5 (GAS5) on spermidine (SP)‑induced autophagy. Pulmonary artery endothelial cells (PAECs) were collected from patients with CTEPH and the rat model. Immunofluorescence, Western blots, reverse transcription‑quantitative polymerase chain reaction, bioinformatics, rapid amplification of cDNA ends assays, luciferase reporter assays, RNA‑binding protein immunoprecipitation assays, GFP‑LC3 adenoviruses, tfLC3 assays and transmission electron microscopy were performed. The results revealed that SP‑induced autophagy increased GAS5 in PAECs. The upregulation of GAS5 enhanced and the downregulation of GAS5 reversed the roles of SP in PAECs. Furthermore, GAS5 promoted SP‑induced autophagy in PAECs by targeting miRNA‑31‑5p. The miRNA‑31‑5p mimic suppressed and the inhibitor promoted SP‑induced autophagy. Furthermore, N‑Acetyltransferase 8 Like (NAT8L) was a target gene of miRNA‑31‑5p and knockdown of NAT8L inhibited the autophagic levels of PAECs.
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