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MicroRNA-27b alleviates septic cardiomyopathy by targeting the Mff/MAVS axis

Xincai Wang1, Long Huang1, Jingqing Xu1

  • 1Department of Critical Care Medicine, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fujian Provincial Hospital, Fujian Provincial Center for Critical Care Medicine, Fujian Provincial Key Laboratory of Critical Care Medicine, Fuzhou, China.

Frontiers in Cellular and Infection Microbiology
|August 6, 2025
PubMed
Abstract

Insights

MicroRNA-27b (miR-27b) protects against septic cardiomyopathy (SCM) by targeting the Mff/MAVS pathway. This finding highlights miR-27b as a potential therapeutic target for SCM.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Mitochondrial Biology

Background:

  • Septic cardiomyopathy (SCM) is a severe complication of sepsis, characterized by cardiac dysfunction and myocardial injury.
  • Mitochondrial dysfunction plays a critical role in the pathogenesis of SCM.
  • The role of microRNAs in regulating mitochondrial dynamics and inflammation in SCM remains incompletely understood.

Purpose of the Study:

  • To investigate the protective role of microRNA-27b (miR-27b) in septic cardiomyopathy (SCM).
  • To elucidate the regulatory mechanism of miR-27b on the mitochondrial fission factor (Mff)/mitochondrial antiviral signaling protein (MAVS) axis in SCM.

Main Methods:

  • Analysis of transcriptome data from septic patient cardiac tissues (GSE79962).
  • Measurement of serum miR-27b levels in SCM patients, sepsis patients, and healthy controls.
  • Establishment of mouse SCM and HL-1 cardiomyocyte models induced by lipopolysaccharide (LPS).
  • Investigation of molecular mechanisms using miR-27b modulators and Mff intervention, coupled with RT-qPCR, Western blot, immunofluorescence, and electron microscopy.

Main Results:

  • Downregulation of miR-27b was observed in SCM cardiac tissues and serum.
  • LPS-induced SCM models exhibited cardiac dysfunction, myocardial injury, and mitochondrial abnormalities.
  • miR-27b targeted Mff, maintaining mitochondrial homeostasis and attenuating LPS-induced inflammation and apoptosis; Mff overexpression reversed these effects.

Conclusions:

  • miR-27b alleviates myocardial injury and inflammation in SCM by targeting the Mff/MAVS axis.
  • Maintaining mitochondrial homeostasis via miR-27b offers a potential therapeutic strategy for SCM.
  • miR-27b represents a promising novel therapeutic target for SCM.
Keywords:
inflammationmicroRNA-27bmitochondrial antiviral signaling proteinmitochondrial fission factorseptic cardiomyopathy

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