Qi-Blood Harmony Formula mediates post-MI cardioprotection via FTO-driven dual modulation of energy metabolism and fibrosis: a multi-omics validation.
7 affiliations
- 1School of Pharmacy, Faculty of Medicine, Macau University of Science and Technology, Macau, 999078, SAR, China.
- 2Laboratory of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
- 3Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
- 4Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China.
- 5Laboratory of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China. [email protected].
- 6School of Pharmacy, Faculty of Medicine, Macau University of Science and Technology, Macau, 999078, SAR, China. [email protected].
- 7Laboratory of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China. [email protected].
Abstract
Myocardial infarction (MI) remains a leading cause of death worldwide. Persistent myocardial fibrosis and dysregulated energy metabolism following MI contribute to adverse cardiac remodeling and are associated with poor clinical prognosis. Currently, no guideline-recommended therapy provides effective long-term intervention simultaneously targeting both of these core pathological mechanisms. The Qi-Blood Harmony Formula (QBHF), a classical Chinese herbal prescription, has demonstrated cardioprotective potential on attenuating fibrosis, preserving mitochondrial integrity, and restoring myocardial ATP levels in MI, yet its underlying mechanisms and therapeutic targets remain unclear. Using an integrated multi-omics approach in a mouse MI model, we showed that QBHF reactivated genes related to energy metabolism while suppressing pro-fibrotic pathways, as revealed by bulk RNA-sequencing. Non-targeted metabolomics further confirmed its efficacy in counteracting metabolic dysregulation. Single-nucleus RNA sequencing revealed that QBHF altered cardiac cellular composition characterized by reducing a major profibrotic fibroblast subpopulation and expanding a metabolically robust cardiomyocyte subset. Integrative multi-omics analysis identified the fat mass and obesity-associated protein (FTO) as a central regulatory hub modulated by QBHF across bulk heart tissue, fibroblasts, and cardiomyocytes. Crucially, heterozygous knockout of FTO in mice abolished QBHF-mediated improvements in cardiac fibrosis, ATP level and heart function. Consistently, FTO knockdown in cardiomyocytes blunted QBHF-induced ATP restoration. Together, these findings demonstrate that QBHF confers post-MI cardioprotection via FTO-driven dual modulation of energy metabolism and fibrosis. Our findings highlight FTO as a promising therapeutic target and provide novel mechanistic insights into traditional Chinese medicine-based interventions for post-MI injury.
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BibTeX
@article{xie2026qiblood,
title = {{Qi-Blood Harmony Formula mediates post-MI cardioprotection via FTO-driven dual modulation of energy metabolism and fibrosis: a multi-omics validation.}},
author = {Xuena Xie and Yuying Wang and Xiaonan Dong and Rong Yuan and Yu Miao and Pengqi Li and Zhitao Wang and Caizhen Zhu and Han Zhao and Lantian Hu and Mei Liu and Zihan Li and Meiwen Huang and Shudong Ma and Qiqi Xin and Weihong Cong and Keji Chen},
journal = {Chinese medicine},
year = {2026},
month = nov,
doi = {10.1186/s13020-026-01506-w},
url = {https://europepmc.org/article/MED/42968160},
note = {CC BY},
}
RIS
TY - JOUR
TI - Qi-Blood Harmony Formula mediates post-MI cardioprotection via FTO-driven dual modulation of energy metabolism and fibrosis: a multi-omics validation.
AU - Xuena Xie
AU - Yuying Wang
AU - Xiaonan Dong
AU - Rong Yuan
AU - Yu Miao
AU - Pengqi Li
AU - Zhitao Wang
AU - Caizhen Zhu
AU - Han Zhao
AU - Lantian Hu
AU - Mei Liu
AU - Zihan Li
AU - Meiwen Huang
AU - Shudong Ma
AU - Qiqi Xin
AU - Weihong Cong
AU - Keji Chen
PY - 2026
DA - 2026/11/02
JO - Chinese medicine
DO - 10.1186/s13020-026-01506-w
UR - https://europepmc.org/article/MED/42968160
AB - Myocardial infarction (MI) remains a leading cause of death worldwide. Persistent myocardial fibrosis and dysregulated energy metabolism following MI contribute to adverse cardiac remodeling and are associated with poor clinical prognosis. Currently, no guideline-recommended therapy provides effective long-term intervention simultaneously targeting both of these core pathological mechanisms. The Qi-Blood Harmony Formula (QBHF), a classical Chinese herbal prescription, has demonstrated cardioprotective potential on attenuating fibrosis, preserving mitochondrial integrity, and restoring myocardial ATP levels in MI, yet its underlying mechanisms and therapeutic targets remain unclear. Using an integrated multi-omics approach in a mouse MI model, we showed that QBHF reactivated genes related to energy metabolism while suppressing pro-fibrotic pathways, as revealed by bulk RNA-sequencing. Non-targeted metabolomics further confirmed its efficacy in counteracting metabolic dysregulation. Single-nucleus RNA sequencing revealed that QBHF altered cardiac cellular composition characterized by reducing a major profibrotic fibroblast subpopulation and expanding a metabolically robust cardiomyocyte subset. Integrative multi-omics analysis identified the fat mass and obesity-associated protein (FTO) as a central regulatory hub modulated by QBHF across bulk heart tissue, fibroblasts, and cardiomyocytes. Crucially, heterozygous knockout of FTO in mice abolished QBHF-mediated improvements in cardiac fibrosis, ATP level and heart function. Consistently, FTO knockdown in cardiomyocytes blunted QBHF-induced ATP restoration. Together, these findings demonstrate that QBHF confers post-MI cardioprotection via FTO-driven dual modulation of energy metabolism and fibrosis. Our findings highlight FTO as a promising therapeutic target and provide novel mechanistic insights into traditional Chinese medicine-based interventions for post-MI injury.
SN - 1749-8546
ER -