ArticleMolecular medicine reports2019
Downregulation of miR‑98 contributes to hypoxic pulmonary hypertension by targeting ALK1.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- MicroRNA-98: the multifaceted regulator in human cancer progression and therapy.Cancer cell international · 2024Review
- Exploring the pathogenesis of pulmonary vascular disease.Frontiers in medicine · 2024Review
- Unraveling the epigenetic landscape of pulmonary arterial hypertension: implications for personalized medicine development.Journal of translational medicine · 2023Review
- miR-155-5p regulates hypoxia-induced pulmonary artery smooth muscle cell function by targeting PYGL.Bioengineered · 2022Article
- Sex Dimorphism in Pulmonary Hypertension: The Role of the Sex Chromosomes.Antioxidants (Basel, Switzerland) · 2021Review
- Genetic Delivery and Gene Therapy in Pulmonary Hypertension.International journal of molecular sciences · 2021Review
- Non-Coding RNA Networks in Pulmonary Hypertension.Frontiers in genetics · 2021Review
- LncRNA ENST00000563492 promoting the osteogenesis-angiogenesis coupling process in bone mesenchymal stem cells (BMSCs) by functions as a ceRNA for miR-205-5p.Cell death & disease · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hypoxia is one of the most common causes of secondary pulmonary hypertension, the mechanisms of which remain unclear. MicroRNAs (miRNAs) are small, noncoding RNAs that inhibit the translation or accelerate the degradation of mRNA. Previous studies have demonstrated that deregulated miRNA expression contributes to various cellular processes including cell apoptosis and proliferation, which are mediated by hypoxia. In the present study, the expression of miR‑98 was identified to be decreased in the lung tissue of a hypoxic pulmonary hypertension (HPH) rat model and pulmonary artery (PA) smooth muscle cells (PASMCs), which was induced by hypoxia. By transfecting miR‑98 mimics into PASMCs, the high expression of miR‑98 inhibited cell proliferation, but upregulated hypoxia‑induced PASMCs apoptosis. However, these effects of miR‑98 mimics on PASMCs were reversed by ALK1 (activin receptor‑like kinase‑1) overexpression. ALK1 was identified as a candidate target of miR‑98. In addition, overexpressing miR‑98 markedly decreased the pulmonary artery wall thickness and the right ventricular systolic pressure in rats induced by hypoxia. These results provided clear evidence that miR‑98 was a direct regulator of ALK1, and that the downregulation of miR‑98 contributed to the pathogenesis of HPH. These results provide a novel potential therapeutic strategy for the treatment of HPH.
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