Liuli Wu,1,* Junchao Huang,2,* Xiongfei Jia,3 Xiaoqin Mao1 

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; 2Department of Clinical Laboratory, Yunnan New Kunhua Hospital, Kunming, Yunnan, 650000, People’s Republic of China; 3Department of Clinical Laboratory, 920th Hospital of Joint Logistics Support Force of Chinese People’s Liberation Army, Kunming, Yunnan, 650000, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Xiaoqin Mao, Department 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, Email maoxq_123@163.com Xiongfei Jia, Department of Clinical Laboratory, 920th Hospital of Joint Logistics Support Force of Chinese People’s Liberation Army, Kunming, Yunnan, 650000, People’s Republic of China, Email saoscm@163.com

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 Ca2+ disturbances caused by septic myocardial injury. This ultimately reduces cellular damage and alleviates septic myocardial injury.

Keywords: septic myocardial injury, MRPS16, MRPL47, mitochondrial function