ArticleJournal of inflammation research2025
Role and Mechanism of Mitochondrial Ribosomal Proteins in Septic Myocardial Injury.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Multi-Organ Physiologic Deficits During Exercise Identify Clinical and Molecular Predisposition to Heart Failure with Preserved Ejection Fraction.Circulation · 2026Article
- Piezo1 knockdown activates PI3K/AKT and enhances SPP1 to drive M2 macrophage polarization and reduce cardiac inflammation.Scientific reports · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To investigate the role of mitochondrial ribosomal proteins (MRPs) in the pathogenesis and progression of septic myocardial injury. Additionally, we aim to propose new technical strategies and experimental foundations for the prevention and treatment of septic myocardial injury. Methods: Animal and cell models of septic myocardial injury were established. Aberrantly expressed MRPs were screened using transcriptome sequencing, and their expression was verified by RT-qPCR and Western blot. Subsequently, overexpressed and knockdown cell models of myocardial injury were constructed. The effects on CO I, PGC-1α, ATP content, ROS fluorescence intensity, mitochondrial membrane potential, and GSDMD were assessed, along with changes in caspase-4 and IL-1β expression levels. Results: Transcriptome sequencing revealed a reduction in MRPs expression in mice with septic myocardial injury. Both RT-qPCR and Western blot analysis confirmed the decreased expression of MRPs in animal and cell models of septic myocardial injury. Furthermore, overexpression of both MRPS16 and MRPL47 mitigated the decrease in CO I and PGC-1α levels induced by septic myocardial injury. Additionally, overexpression of MRPS16 and MRPL47 alleviated the elevated levels of IL-1β, caspase-4, and GSDMD caused by septic myocardial injury. Conclusion: The findings suggest that both MRPS16 and MRPL47 can mitigate mitochondrial injury by attenuating mitochondrial biosynthesis dysfunction, energy metabolism disorders, and Ca
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