Open Access

REVIEW

How Do LncRNAs Talk to miRNAs? Decoding Their Dialogue in Atherosclerosis

Yating Wei¹, Hongkang Yao¹, Xian Shi², Hong Chen³, Rongzong Ye^4,*, Chaoqian Li^1,*

1 Department of Emergency Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530000, China
2 Department of Genomic Function and Diversity, Graduate School of Medical and Dental Sciences, Tokyo Institute of Science, Tokyo, 162-8601, Japan
3 Department of Cardiology, Guangxi Medical University, Nanning, 530000, China
4 Department of Critical Care Medicine, The First Affiliated Hospital of Xiamen University, Xiamen, 361000, China

* Corresponding Authors: Rongzong Ye. Email: ; Chaoqian Li. Email:

(This article belongs to the Special Issue: Advanced Cell Signaling Pathways in Health and Disease)

BIOCELL 2026, 50(2), 5 https://doi.org/10.32604/biocell.2025.072780

Received 03 September 2025; Accepted 31 October 2025; Issue published 14 February 2026

Abstract

Atherosclerosis, characterized by the formation of fibrofatty lesions in the arterial wall, remains a leading cause of global morbidity and mortality. Emerging evidence highlights the critical regulatory roles of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in atherogenesis. LncRNAs can function as competing endogenous RNAs (ceRNAs) by sponging miRNAs, thereby modulating the expression of downstream target mRNAs. This review summarizes current knowledge on lncRNA-miRNA-mRNA regulatory networks and their functional roles in the three major cell types involved in atherosclerotic plaque development: endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and macrophages. In ECs, these networks are implicated in inflammation, apoptosis, proliferation, angiogenesis, pyroptosis, and autophagy. In VSMCs, they regulate proliferation, apoptosis, and migration. In macrophages, they influence lipid metabolism, inflammatory responses, oxidative stress, and autophagy. Although the ceRNA mechanism is predominant, some lncRNAs also act as primary transcripts for miRNAs. Additionally, exosome-mediated non-coding RNA delivery mediates intercellular crosstalk, further expanding the complexity of RNA-based regulation in atherosclerosis. Despite significant progress, challenges remain due to the complexity and context-specificity of these networks. Further research is essential to elucidate these mechanisms and explore their potential as therapeutic targets for atherosclerosis.

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Keywords

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