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Updated: Jun 4, 2025
Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
Mmu_circ_0001148 promotes endothlial-mesenchymal transition via regulating miR-218-5p/JMY axis and drives progression
Shang-Min Yu1, Jia-Qi Liu2, Lin-Lin Zhang3
1Department of Pharmaceutics, School of Pharmacy, Bengbu Medical University, Bengbu 233000, Anhui, China.
Insights
A novel circular RNA, circ_0001148, promotes atherosclerosis by inducing endothelial-mesenchymal transition. It acts as a ceRNA, sponging miR-218-5p to regulate JMY, offering a potential therapeutic target for cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- RNA Biology
Background:
- Atherosclerosis (AS) is a major cause of cardiovascular mortality.
- Circular RNAs (circRNAs) are implicated in AS pathogenesis.
- The role of circ_0001148 in AS requires elucidation.
Purpose of the Study:
- Investigate the function of circ_0001148 in AS.
- Elucidate the underlying molecular mechanism of circ_0001148 in AS.
- Explore circ_0001148 as a potential therapeutic target.
Main Methods:
- Identification of aberrantly expressed circRNA in atherosclerotic tissues.
- Functional analysis of circ_0001148's role in endothelial-mesenchymal transition (EndMT).
- Mechanism analysis involving competitive endogenous RNA (ceRNA) interactions (circ_0001148/miR-218-5p/JMY axis).
Main Results:
- circ_0001148 promotes EndMT and accelerates atherosclerotic plaque formation.
- circ_0001148 functions as a ceRNA, sponging miR-218-5p to regulate JMY expression.
- Overexpression of circ_0001148-induced AS progression was attenuated by miR-218-5p mimics or JMY deficiency.
Conclusions:
- A novel signaling network: circ_0001148 promotes atherogenesis via the miR-218-5p/JMY axis.
- circ_0001148 plays a significant role in AS development.
- This pathway presents a potential therapeutic strategy for atherosclerosis.
Abstract:
Atherosclerosis (AS) is a common cardiovascular disease and responsible for the high mortality of cardiovascular emergencies. Circular RNAs (circRNAs) show a potential role in atherogenesis. We identified an aberrantly expressed circRNA (circ_0001148) in atherosclerotic tissues. However, whether circ_0001148 involved in atherogenesis remains unclear. The present study aimed to investigate the biological function of circ_0001148 and the underlying mechanism in AS. Functional analysis indicated that circ_0001148 promoted endothelial-mesenchymal transition (EndMT) and thus accelerated the formation of atherosclerotic plaque. The mechanism analysis suggested that circ_0001148 act as a competitive endogenous RNA (ceRNA) to modify the expression of JMY by sponging miR-218-5p. We also demonstrated that the treatment of miR-218-5p mimics or JMY deficiency could attenuated the progression of AS induced by circ_0001148 overexpression. Therefore, we proposed a novel signaling network which circ_0001148 promotes atherogenesis via miR-218-5p/JMY axis. These findings provide new insights into the mechanisms of AS, and potentially leading to the development of a novel therapeutic strategy targeting circ_0001148.
