ArticleJournal of advanced research2025
Novel long noncoding lncARF mediated hyperhomocysteinemia-induced atherosclerosis via autophagy inhibition in foam cells.
Article in Journal of advanced research, 2025. 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.
- Maternal hyperhomocysteinemia compromises female offspring fertility through overactivation of primordial follicles.iScience · 2026Article
- Non-canonical ceRNA-independent mechanism of the lncRNA-H19/miR-212-5p axis targeting KLF4 in Hcy-triggered VSMCs dysfunction and atherogenesis.Scientific reports · 2026Article
- PI3K/AKT signaling pathway: new strategies for treating atherosclerosis with plant-derived compounds.Frontiers in pharmacology · 2026Review
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- DNA hypomethylated modified lncRNA MALAT1 promotes atherosclerotic cardiovascular disease progression through NF-κB signaling pathway regulating cholesterol metabolism and inflammatory response.Biochemistry and biophysics reports · 2025Article
- Biomimetic membrane-coated nanoparticles for targeted synergistic therapy of homocysteine-induced atherosclerosis: Dual modulation of cholesterol efflux and reactive oxygen species scavenging.Materials today. Bio · 2025Article
- Heart Failure and Gut Microbiota: What Is Cause and Effect?Research (Washington, D.C.) · 2025Review
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Authors and funding
11 authors.
Funding
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Abstract
introductionHomocysteine (Hcy) is well recognized to be an independent risk factor for atherosclerosis. Long non-coding RNAs (lncRNAs) are emerging regulators of pathophysiological processes including atherosclerosis, while the underlying mechanisms of its involvement in Hcy induced-atherosclerosis remain largely unknown.
objectivesThe primary aim of this study is to assess the role of lncARF (autophagy-related factor induced by Hcy) in Hcy induced-atherosclerosis and related mechanism.
methodsRNA sequencing of foam cells treated with Hcy revealed a novel specific long noncoding RNA called lncARF. Locked nucleic acid gapmeRs-mediated lncARF knockdown was used to explore the role of lncARF both in vivo and in vitro. Mass spectrometry, RNA pull-down and RNA immunoprecipitation (RIP) assays were employed to uncover a mechanistic role of lncARF. Mass array assay and chromatin immunoprecipitation (ChIP) were used to detect the transcriptional activation of lncARF mediated by transcription factor. Clinically, receiver operating characteristic (ROC) curve analysis was used to assess the diagnostic value of lncARF in atherosclerotic patients with hyperhomocysteinemia (HHcy).
resultsWe observed that the expression of lncARF was substantially upregulated in atherosclerotic plaques, and knockdown of lncARF decreased the formation of atherosclerotic lesions by promoting autophagy in foam cells. Mechanistically, lncARF physically binds to RRAGD and inhibits its ubiquitination, further activating the PI3K/Akt and MAPK signaling pathways. Moreover, in vitro experiments showed that transcription factor FosB inhibited the binding of DNMT1 at the lncARF promoter, leading to transcriptional activation through DNA hypomethylation. Clinically, lncARF expression was positively correlated with serum Hcy levels, and it could distinguish atherosclerotic patients with HHcy with a high area under the ROC curve, sensitivity and specificity.
conclusionsOur study highlights the mechanisms of lncARF in protecting against the development of atherosclerosis involving the epigenetic modifications and RRAGD/PI3K/Akt and RRAGD/MAPK signaling pathways, which may provide novel diagnostic biomarkers to improve atherosclerosis treatment.
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