ArticleBioscience reports2019
LncRNA LOXL1-AS is up-regulated in thoracic aortic aneurysm and regulated proliferation and apoptosis of aortic smooth muscle cells.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Emerging Roles of Long Non-Coding RNAs in Cardiovascular Diseases.Journal of cellular and molecular medicine · 2025Review
- Multi-omics in thoracic aortic aneurysm: the complex road to the simplification.Cell & bioscience · 2023Review
- Article
- The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections.European journal of clinical investigation · 2022Review
- Weighted miRNA co-expression network reveals potential roles of apoptosis related pathways and crucial genes in thoracic aortic aneurysm.Journal of thoracic disease · 2021Article
- The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage.Life (Basel, Switzerland) · 2020Review
- LncRNA Sox2ot modulates the progression of thoracic aortic aneurysm by regulating miR-330-5p/Myh11.Bioscience reports · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Long non-coding RNA LOXL1-AS is up-regulated in several types of cancers. The present study was carried out to explore the potential interactions between LOXL1-AS and lncRNA Giver in thoracic aortic aneurysm (TAA). We found that LOXL1-AS was up-regulated in TAA patients than in healthy controls in aortic media specimens. Altered expression levels of LOXL1-AS distinguished TAA patients from healthy controls. LncRNA Giver was also up-regulated in TAA patients than in healthy controls in aortic media specimens, and was positively correlated with LOXL1-AS. LOXL1-AS overexpression mediated the up-regulation of Giver in human aortic smooth muscle cells, while Giver overexpression failed to significantly affect LOXL1-AS. LOXL1-AS and Giver overexpression resulted in promoted proliferation and inhibited apoptosis of HAOSMC. Giver silencing played an opposite role and attenuated the effect of LOXL1-AS overexpression. Therefore, LOXL1-AS was up-regulated in TAA and regulated proliferation and apoptosis of LOXL1-AS by up-regulating Giver.
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