ArticleScientific reports2022
LncRNA ANRIL-mediated miR-181b-5p/S1PR1 axis is involved in the progression of uremic cardiomyopathy through activating T cells.
Article in Scientific reports, 2022. 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, 10 citations in OpenAlex.
- ANRIL in Cardiovascular Diseases: Expression, Mechanism and Therapeutic Implications.Cardiovascular drugs and therapy · 2026Review
- Salvianolic Acid B Upregulates miR-744-5p Expression in Peripheral Blood Mononuclear Cell-Derived Extracellular Vesicles to Alleviate Uremic Cardiomyopathy.Journal of extracellular vesicles · 2026Article
- Long non-coding RNAs as molecular hubs integrating inflammatory and osteogenic pathways in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2026Review
- Review
- Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025Review
- Screening and identification of hub genes for ischemic cardiomyopathy and construction and validation of a clinical prognosis model using bioinformatics analysis.Journal of thoracic disease · 2024Article
- Panax notoginseng saponins inhibits NLRP3 inflammasome-mediated pyroptosis by downregulating lncRNA-ANRIL in cardiorenal syndrome type 4.Chinese medicine · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
This study aimed to explore the regulatory role of lncRNA ANRIL/miR-181b-5p/S1PR1 in UC. UC mouse model was established by 5/6th nephrectomy. We detected body weight, serum levels of renal function and inflammatory factors (biochemical analyzer/ELISA), and cardiac parameters (echocardiography). HE and Masson staining showed the pathological changes and fibrosis in myocardial and nephridial tissues. The expression of ANRIL, miR-181b-5p, and S1PR1 were detected by qRT-PCR or Western blot/immunofluorescence. T cells activation was analyzed by Flow cytometry. ANRIL/S1PR1 were up-regulated and miR-181b-5p was down-regulated in UC mice. ANRIL silencing up-regulated miR-181b-5p and down-regulated S1PR1 (a target of miR-181b-5p). ANRIL silencing increased the body weight, recovered renal function [decreased blood urea nitrogen (BUN) and serum creatinine (Scr)] and cardiac function [decreased left ventricular end-diastolic diameter (LVEDD), LV end-systolic diameter (LVESD), LV systolic anterior wall thickness (LVAWS), LV end-diastolic anterior wall thickness (LVAWD), myocardial performance index (MPI), and isovolumic relaxation time (IVRT); increased LV ejection fraction (LVEF), LVEF/MPI, fractional shortening (FS), and E- and A-waves (E/A)], inhibited the inflammation [decreased interferon (IFN)-γ, interleukin (IL)-2, IL-10, and tumor necrosis factor (TNF)-α], and relieved pathological injuries and fibrosis. ANRIL silencing also recovered the viability and inhibited the inflammation of activated T cells in vitro, and inhibited T cell activation in UC mice in vivo. In addition, miR-181b-5p overexpression exhibited same effects with ANRIL silencing in UC. ANRIL silencing inhibited T cell activation through regulating miR-181b-5p/S1PR1, contributing to the remission of UC.
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