Front. Genet. Frontiers in Genetics Front. Genet. 1664-8021 Frontiers Media S.A. 1746339 10.3389/fgene.2025.1746339 Correction Correction: Non-coding RNAs in heart failure: epigenetic regulatory mechanisms and therapeutic potential Ren et al. 10.3389/fgene.2025.1746339 Ren Yubo 1 Writing - original draft Conceptualization Resources Visualization Writing - review and editing Zhao Bomeng 1 Conceptualization Visualization Writing - original draft Writing - review and editing Lv Luo 2 Validation Writing - review and editing Yang Jingyuan 1 Visualization Writing - review and editing Nan Xiangting 3 Writing - review and editing Li Bao 4 5 * Conceptualization Writing - original draft Yang Bin 4 5 * Conceptualization Writing - review and editing Second College of Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, China The First College of Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, China Shanxi Medical University, Taiyuan, Shanxi, China Department of Cardiology, The Second Hospital of Shanxi Medical University, Taiyuan, China School of Medicine, Shanxi Medical University, Taiyuan, China Correspondence: Bao Li, libaoxys@163.com; Bin Yang, yangbxys@163.com 24 11 2025 2025 16 1746339 14 11 2025 14 11 2025 17 11 2025 Copyright © 2025 Ren, Zhao, Lv, Yang, Nan, Li and Yang. 2025 Ren, Zhao, Lv, Yang, Nan, Li and Yang https://creativecommons.org/licenses/by/4.0/ 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) and the copyright owner(s) 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. A Correction on Non-coding RNAs in heart failure: epigenetic regulatory mechanisms and therapeutic potential by Ren Y, Zhao B, Lv L, Yang J, Nan X, Li B and Yang B (2025). Front. Genet. 16:1677797. doi: 10.3389/fgene.2025.1677797 heart failure non-coding RNA epigenomics microRNAs long non-coding RNA circular RNA therapeutics section-in-acceptance RNA

There was a mistake in Figure 4 as published. In Figure 4, the word “faiure” was incorrectly spelled. The correct spelling is “failure.” The corrected Figure 4 appears below.

Differential ncRNA Expression in HF Types. This figure outlines the characteristic ncRNAs signatures across in patients with different types of HF. The pathogenesis and diagnoses depicted are all related to heart failure. The potential biomarkers mentioned require validation through large-scale, multi-center clinical trials. This does not imply that these biomarkers are without impact on the disease pathogenesis. (A) In HFrEF, miR-375 and lncRNA GDE1-1:1 are downregulated, while miR-208, miR-423-5p, exo-miR-92b-5p, lncRNA SRA1, lncRNA HEAT2, and circRNA DEPCS are upregulated. These molecules are potential biomarkers for HFrEF diagnosis. (B) In HFpEF, miR-19b-3p is downregulated, while miR-222/221, lncRNA TUG1, lncRNA MHRT, and circRNA HECW2 are upregulated. These molecules serve as potential biomarkers for HFpEF, with lncRNA XIST and circRNA HECW2 linked to profibrotic and inflammatory pathways. The figure is created in https://BioRender.com.

Chart illustrating molecular markers in heart failure subtypes HFrEF and HFpEF. miRNAs such as miR-375 and miR-19b-3p are downregulated, while miR-208 and miR-221/222 are upregulated. lncRNAs SRA1, HEAT2, TUG1, MHRT, and XIST show upregulation or downregulation. circRNAs DEPCS and HECW2 are upregulated. Each marker's regulation direction is marked with arrows.

There was a mistake in Figure 5 as published. In Figure 5, the words “faiure” and “diabete” were incorrectly spelled. The correct spellings are “failure” and “diabetes,” respectively. The corrected Figure 5 appears below.

Differential ncRNA Expression in HF Comorbidities and Complications. This figure illustrates the characteristic ncRNA signatures in patients with HF and its comorbidities and complication. The potential biomarkers highlighted need to be validated through large-scale, multi-center clinical trials. This does not suggest that these biomarkers are irrelevant to the disease process. (A) In HF patients with CAD, miR-132 and lncRNA ANRIL are upregulated, contributing to the pathogenesis of CAD. miR-208a/β is also upregulated, helping diagnose myocardial injury alongside troponin. (B) In HF patients with diabetes, miR-34a is upregulated and miR-21 is downregulated, both serving as biomarkers for HFrEF. lncRNA MALAT1 is upregulated, increasing myocardial apoptosis and fibrosis. LncRNA KCNQ1OT1 is also upregulated, promoting cardiomyocyte pyroptosis and fibrosis. lncRNA HOTAIR is downregulated, promoting cardiac oxidative stress. (C) In HF patients with AF, lncRNA UCA1 is upregulated, promoting myocardial hypertrophy. lncRNA SARRAH is downregulated in atrial tissue but upregulated in serum, linked to resistance to oxidative stress and ischemic injury. (D) In HF patients with obesity, miR-33 and miR-122 are both upregulate. miR-122 promotes cardiac hypertrophy and fibrosis. miR-33 Participates in cardiovascular remodeling. The figure is created in https://BioRender.com.

Diagram illustrating heart failure with associated conditions and molecular markers. Conditions include CAD, diabetes, AF, and obesity. Molecular markers include upregulated miRNAs (miR-132, miR-208a/β, miR-34a, miR-122, miR-33) and downregulated miRNA (miR-21). lncRNAs include ANRIL, MALAT1, KCNQ1OT1, UCA1, and SARRAH, with differential expression in tissues or serum.

The original article has been updated.

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