• Xiaocong Liu, Siyu Chen, Wei Luo, Chen Yu, Shaohua Yan, Li Lei, Shifeng Qiu, Xinxin Lin, Ting Feng, Jinglin Shi, Qiuxia Zhang, Hongbin Liang, Xuewei Liu, Alex Pui-Wai Lee, Lei Zheng, Xinlu Zhang, and Jiancheng Xiu.
• Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, PR China.
• Transl Res. 2024 Oct 1; 272: 546754-67.

BackgroundArterial remodeling is a common pathophysiological change in the pathogenesis of cardiovascular diseases in which the phenotypic switch of vascular smooth muscle cells (VSMC) plays an important role. Recently, an increasing number of long non-coding RNAs(lncRNAs) have been shown to encode micropeptides that play biological roles and have great clinical transformation potential. However, the role of micropeptides encoded by lncRNAs in arterial remodeling has not been well studied and requires further exploration.Methods And ResultsThrough bioinformatic analysis and experimental verification, we found that a new lncRNA, the mitochondrial function-related lncRNA (MFRL), encodes a 64-amino acid micropeptide, MFRLP. MFRL and MFRLP play important roles in the phenotypic switch of VSMC. Further experiments showed that MFRLP interacts with mitochondrial cytochrome b to reduce accumulation of reactive oxygen species, suppress mitophagy and inhibit the VSMC switch from contractile to synthetic phenotype.ConclusionsLncRNA MFRL encodes the micropeptide MFRLP, which interacts with mitochondrial cytochrome b to inhibit the VSMC switch from contractile to synthetic phenotype and improve arterial remodeling.Copyright © 2024 Elsevier Inc. All rights reserved.

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