ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Clinical Infectious Diseases
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1588461
This article is part of the Research TopicMolecular mechanisms and clinical studies of multi-organ dysfunction in sepsis associated with pathogenic microbial infectionView all 19 articles
MicroRNA-27b Alleviates Septic Cardiomyopathy by Targeting the Mff/MAVS Axis
Provisionally accepted
- 1Department of Critical Care Medicine, Fujian Provincial Hospital, Fuzhou, Fujian Province, China
- 2Fujian Medical University, Fuzhou, Fujian Province, China
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Objective: To investigate the protective role of microRNA-27b (miR-27b) in septic cardiomyopathy (SCM) and its regulatory mechanism on the mitochondrial fission factor (Mff)/mitochondrial antiviral signaling protein (MAVS) axis.: Transcriptome data from septic patients' cardiac tissues (GSE79962) were analyzed. Serum miR-27b expression was measured in SCM patients (n=11), sepsisonly patients (n=22), and healthy controls (n=30). Mouse SCM model and HL-1 cardiomyocyte model were established by lipopolysaccharide (LPS) induction. The molecular mechanism was investigated using miR-27b agonist/antagonist and Mff intervention, combined with RT-qPCR, Western blot, immunofluorescence, and transmission electron microscopy. Results: Bioinformatics analysis revealed significant downregulation of miR-27b in SCM cardiac tissues (log2FC=-3.9, P<0.001). Clinical validation showed lower miR-27b expression in SCM patients' serum compared to sepsis-only patients and healthy controls (P<0.05). LPS-induced SCM model exhibited cardiac dysfunction, myocardial injury, mitochondrial abnormalities, decreased miR-27b expression, and increased Mff and MAVS levels. miR-27b targeted Mff to maintain mitochondrial homeostasis, thus attenuating LPS-induced cardiomyocyte inflammation and apoptosis, while Mff overexpression reversed this protective effect. 2 Conclusion: miR-27b alleviates myocardial injury and inflammation in SCM by targeting the Mff/MAVS axis to maintain mitochondrial homeostasis, representing a potential novel therapeutic target for SCM.
Keywords: Inflammation, microRNA-27b, Mitochondrial antiviral signaling protein, mitochondrial fission factor, septic cardiomyopathy LPS: lipopolysaccharide, LVEF: Left ventricular ejection fraction, MAVS: mitochondrial antiviral signaling protein, Mff: mitochondrial fission factor
Received: 05 Mar 2025; Accepted: 30 Jun 2025.
Copyright: © 2025 Wang, Huang, Xu, Li, Zhang, Yao, Liu and Shang. 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: Xiuling Shang, Department of Critical Care Medicine, Fujian Provincial Hospital, Fuzhou, Fujian Province, China
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