ORIGINAL RESEARCH article
Front. Cell Dev. Biol.
Sec. Stem Cell Research
Volume 13 - 2025 | doi: 10.3389/fcell.2025.1694467
Exosomal lncRNA XR_001793654.1 in human cardiac explant-derived alleviates atrial fibrillation via abolishing the miR-107-3p-mediated KLF13 inhibition
Provisionally accepted
- 1Department of Hematology, Shengjing Hospital of China Medical University, Shenyang, China
- 2General Hospital of Northern Theatre Command, Shenyang, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: Atrial fibrillation (AF) is a type of arrhythmia that occurs in the upper part of the heart. Extracellular vesicles (EVs) released by human cardiac explant-derived cells (CDCs) contain bioactive cargos that may function as diagnostic indicators or therapeutic candidates for AF. The lncRNA XR_001793654.1 has been identified as a putative modulator in AF pathogenesis. Methods: Human CDCs were derived from left atrial appendages collected during cardiac surgery. Then, EVs were isolated from cultured CDCs using ultracentrifugation. XR_001793654.1 expression was quantified in EVs. The relationship between XR_001793654.1, miR-107-3p, and KLF13 was identified. Results: XR_001793654.1 was upregulated in EVs from human CDCs. Systemic delivery of these EVs in vivo diminished atrial fibrosis and hypertrophy, with concurrent suppression of inflammatory cell accumulation and pro-inflammatory cytokine release. Mechanistically, EV-associated XR_001793654.1 served as ceRNA, sequestering miR-107-3p and thereby alleviating its inhibitory regulation of KLF13 expression. Elevation of KLF13 was essential for the observed cardioprotective outcomes. Conclusion: In conclusion, human CDC-derived EV containing XR_001793654.1 alleviates atrial fibrosis and AF through neutralizing miR-107-3p-mediated downregulation of KLF13. These findings offer new perspectives on AF molecular mechanisms and emphasize XR_001793654.1 as a promising intervention target.
Keywords: Atrial Fibrillation, extracellular vesicles, lncRNA XR_001793654.1, miR-107-3p, KLF13
Received: 28 Aug 2025; Accepted: 21 Oct 2025.
Copyright: © 2025 Liang, Li, WANG and Tian. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: HUISHAN WANG, wanghuishan2024@163.com
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.