ArticleFrontiers of medicine2023
lncR-GAS5 upregulates the splicing factor SRSF10 to impair endothelial autophagy, leading to atherogenesis.
Article in Frontiers of medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Exosomal lncRNAs in Cerebrovascular Diseases: Biomarkers, Pathological Mechanisms, and Therapeutic Potential.Non-coding RNA · 2026Review
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- THBru ameliorates atherosclerosis by inhibiting endothelial ferroptosisActa pharmaceutica Sinica. B · 2025Article
- GAS5 Long Noncoding RNA Regulates CD20 Expression and Rituximab Response.Advanced pharmaceutical bulletin · 2025Article
- Unraveling LncRNA GAS5 in Atherosclerosis: Mechanistic Insights and Clinical Translation.Biology · 2025Review
- Recent Advances in the Mutual Regulation of m6A Modification and Non-Coding RNAs in Atherosclerosis.International journal of general medicine · 2025Review
- LncRNA LUCAT1 offers protection against human coronary artery endothelial cellular oxidative stress injury through modulating hsa-miR-6776-5p/LRRC25 axis and activating autophagy flux.Journal of translational medicine · 2024Article
- Regulating the regulators: long non-coding RNAs as autophagic controllers in chronic disease management.Journal of biomedical science · 2024Review
- The novel anthraquinone compound Kanglexin prevents endothelial-to-mesenchymal transition in atherosclerosis by activating FGFR1 and suppressing integrin β1/TGFβ signaling.Frontiers of medicine · 2024Article
- Role of long noncoding RNAs in diabetes-associated peripheral arterial disease.Cardiovascular diabetology · 2024Review
- The role of hsa-miR-193a-5p as an important factor for control of inositol in alopecia areata.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024Review
- The role of splicing events in the inflammatory response of atherosclerosis: molecular mechanisms and modulation.Frontiers in immunology · 2024Review
- Genetic dissection of the impact of lncRNA AI662270 during the development of atherosclerosis.Journal of translational medicine · 2023Article
- Non-coding RNAs are key players and promising therapeutic targets in atherosclerosis.Frontiers in cell and developmental biology · 2023Review
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.
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