Transcriptome expression profiles and regulatory networks in patients with heart failure following myocardial infarction
- 1Department of Cardiology, Anning First People’s Hospital Affiliated to Kunming University of Science and Technology, No.2 Ganghe Rd, Kunming, Yunnan 650300 China
- 2Department of Endocrinology and Metabolic Diseases, Anning First People’s Hospital Affiliated to Kunming University of Science and Technology, No.2 Ganghe Rd, Kunming, Yunnan 650300 China
Abstract
Background: The molecular mechanisms underlying heart failure (HF) following myocardial infarction (MI) (HF-MI) remain incompletely understood, and discoveries from whole-transcriptome profiling hold significant promise for disease prevention and treatment.
Methods: Whole-transcriptome sequencing was performed on whole blood from post-MI patients with and without HF to analyze differentially expressed mRNAs, lncRNAs, and circRNAs, along with functional enrichment analysis. Co-expression networks linking lncRNA-mRNA and circRNA-mRNA pairs, as well as ceRNA networks involving lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA interactions, were constructed for differentially expressed (DE) RNAs. Candidate lncRNAs were validated by RT-qPCR. Transcriptional factor-lncRNA networks were constructed, and candidate relationships were verified using RIP-PCR.
Results: Patients with HF-MI exhibited marked elevation of NT-proBNP and significant reduction in LVEF%. Transcriptome-wide analysis revealed 228 DE-mRNAs, 700 DE-lncRNAs, and 1188 DE-circRNAs in HF-MI compared to non-heart failure patients (NHF-MI). Construction of the ceRNA network identified hsa-miR-6089 and hsa-miR-6771-5p as candidate miRNAs in the lncRNA-miRNA-mRNA network, while hsa-miR-1207-5p and hsa-miR-10392-3p were candidate miRNAs in the circRNA-miRNA-mRNA network. PVT1, SNHG5, TTN-AS1, HCP5, and OIP5-AS1 were identified as the five candidate DE-lncRNAs, with PVT1/SNHG5 showing upregulation and TTN-AS1/HCP5/OIP5-AS1 exhibiting downregulation. The transcription factor-lncRNA network primarily involves GLIS3-HCP5 and ZNF135-PVT1, with validated associative interactions.
Conclusion: This study systematically mapped the regulatory network of HF-MI, suggesting potential involvement of the GLIS3-HCP5 and ZNF135-PVT1 axes in HF-MI, thereby providing a basis for exploring novel therapeutic strategies.
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BibTeX
@article{yuan2026transcriptome,
title = {{Transcriptome expression profiles and regulatory networks in patients with heart failure following myocardial infarction}},
author = {Yangyang Yuan and Rong Long and Zewen Wei and Lin Ye and Jianying Sun and Shouguo Zhu and Zhi Zhang and Jian Li},
journal = {BMC Cardiovascular Disorders},
year = {2026},
month = aug,
doi = {10.1186/s12872-026-06424-1},
url = {https://doi.org/10.1186/s12872-026-06424-1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Transcriptome expression profiles and regulatory networks in patients with heart failure following myocardial infarction
AU - Yangyang Yuan
AU - Rong Long
AU - Zewen Wei
AU - Lin Ye
AU - Jianying Sun
AU - Shouguo Zhu
AU - Zhi Zhang
AU - Jian Li
PY - 2026
DA - 2026/08/12
JO - BMC Cardiovascular Disorders
DO - 10.1186/s12872-026-06424-1
UR - https://doi.org/10.1186/s12872-026-06424-1
AB - Background: The molecular mechanisms underlying heart failure (HF) following myocardial infarction (MI) (HF-MI) remain incompletely understood, and discoveries from whole-transcriptome profiling hold significant promise for disease prevention and treatment. Methods: Whole-transcriptome sequencing was performed on whole blood from post-MI patients with and without HF to analyze differentially expressed mRNAs, lncRNAs, and circRNAs, along with functional enrichment analysis. Co-expression networks linking lncRNA-mRNA and circRNA-mRNA pairs, as well as ceRNA networks involving lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA interactions, were constructed for differentially expressed (DE) RNAs. Candidate lncRNAs were validated by RT-qPCR. Transcriptional factor-lncRNA networks were constructed, and candidate relationships were verified using RIP-PCR. Results: Patients with HF-MI exhibited marked elevation of NT-proBNP and significant reduction in LVEF%. Transcriptome-wide analysis revealed 228 DE-mRNAs, 700 DE-lncRNAs, and 1188 DE-circRNAs in HF-MI compared to non-heart failure patients (NHF-MI). Construction of the ceRNA network identified hsa-miR-6089 and hsa-miR-6771-5p as candidate miRNAs in the lncRNA-miRNA-mRNA network, while hsa-miR-1207-5p and hsa-miR-10392-3p were candidate miRNAs in the circRNA-miRNA-mRNA network. PVT1, SNHG5, TTN-AS1, HCP5, and OIP5-AS1 were identified as the five candidate DE-lncRNAs, with PVT1/SNHG5 showing upregulation and TTN-AS1/HCP5/OIP5-AS1 exhibiting downregulation. The transcription factor-lncRNA network primarily involves GLIS3-HCP5 and ZNF135-PVT1, with validated associative interactions. Conclusion: This study systematically mapped the regulatory network of HF-MI, suggesting potential involvement of the GLIS3-HCP5 and ZNF135-PVT1 axes in HF-MI, thereby providing a basis for exploring novel therapeutic strategies.
SN - 1471-2261
ER -