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Updated: May 25, 2025

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Role and Mechanism of Mitochondrial Ribosomal Proteins in Septic Myocardial Injury

Liuli Wu1, Junchao Huang2, Xiongfei Jia3

  • 1Department of Clinical Laboratory, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, 650500, People's Republic of China.

Journal of Inflammation Research
|February 26, 2025
PubMed
Abstract

Insights

Mitochondrial ribosomal proteins (MRPs), specifically MRPS16 and MRPL47, were found to be reduced in septic myocardial injury. Their restoration mitigated mitochondrial dysfunction and reduced cellular damage, offering therapeutic potential.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiology

Background:

  • Septic myocardial injury is a critical complication of sepsis.
  • Mitochondrial dysfunction plays a key role in the pathogenesis of septic myocardial injury.
  • The specific role of mitochondrial ribosomal proteins (MRPs) in this context remains underexplored.

Purpose of the Study:

  • To investigate the role of MRPs in septic myocardial injury.
  • To identify potential therapeutic targets for preventing and treating septic myocardial injury.
  • To explore novel strategies for managing this condition.

Main Methods:

  • Established animal and cell models of septic myocardial injury.
  • Utilized transcriptome sequencing to screen for aberrantly expressed MRPs.
  • Verified MRP expression via RT-qPCR and Western blot.
  • Constructed overexpressed and knockdown cell models to assess functional impacts.

Main Results:

  • Transcriptome sequencing revealed decreased MRP expression in septic myocardial injury.
  • RT-qPCR and Western blot confirmed reduced MRP levels in both animal and cell models.
  • Overexpression of MRPS16 and MRPL47 counteracted sepsis-induced decreases in CO I and PGC-1α.
  • Overexpression of MRPS16 and MRPL47 reduced elevated IL-1β, caspase-4, and GSDMD levels.

Conclusions:

  • MRPS16 and MRPL47 mitigate mitochondrial injury in sepsis.
  • These proteins attenuate mitochondrial biosynthesis dysfunction and energy metabolism disorders.
  • Restoring MRPS16 and MRPL47 levels reduces cellular damage and alleviates septic myocardial injury.
Keywords:
MRPL47MRPS16mitochondrial functionseptic myocardial injury

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