MicroRNAs as Biomarkers of Mitochondrial Function and Functional Recovery in Critical Illness
Document Type
Abstract
Start Date
28-4-2026 3:30 PM
End Date
28-4-2026 4:45 PM
Description
Diaphragm dysfunction that leads to respiratory failure is a significant clinical consequence of sepsis-induced critical illness. Diaphragm muscle weakness contributes to morbidity and mortality in these individuals in part due to impaired mitochondrial function. Restoring normal mitochondrial biogenesis is associated with improved survival and physical function. Therefore, identifying reliable biomarkers of mitochondrial dysfunction in diaphragm muscle will allow more focused and targeted interventions designed to improve the morbidity of critically ill patients. MicroRNAs—a small class of non-coding RNAs about 22 nucleotides long, and the microRNA regulatory network plays a significant role in skeletal muscle mitochondrial regulation, differentiation, proliferation, and apoptosis. A rodent cecal-ligation and puncture (CLP) model was used to mimic sepsis-induced critical illness. The CLP model involved ligation of 50% of the cecum below the ileocecal valve in adult C57BL6 mice, followed by needle puncture of the cecum resulting in mid-grade sepsis. Mice survived for 48 hours or more, following injury. The diaphragm muscle was harvested from adult mice 48 hours following CLP (N=6) or a sham CLP procedure (N=6). Our primary finding was moderate grade CLP increases expression of mitochondria associated microRNA in the diaphragm. Correspondingly, genes associated with mitochondrial biogenesis decreased. Our study provides evidence for sepsis mediated dysregulation of mitochondrial homeostasis. This may play a role in diaphragm muscle dysfunction, respiratory failure, and difficult weaning from mechanical ventilation in critically ill patients.
Recommended Citation
Gill, Luther, "MicroRNAs as Biomarkers of Mitochondrial Function and Functional Recovery in Critical Illness" (2026). School of Allied Health Professions Research Day. 14.
https://digitalscholar.lsuhsc.edu/ahrd/2026/presentations/14
MicroRNAs as Biomarkers of Mitochondrial Function and Functional Recovery in Critical Illness
Diaphragm dysfunction that leads to respiratory failure is a significant clinical consequence of sepsis-induced critical illness. Diaphragm muscle weakness contributes to morbidity and mortality in these individuals in part due to impaired mitochondrial function. Restoring normal mitochondrial biogenesis is associated with improved survival and physical function. Therefore, identifying reliable biomarkers of mitochondrial dysfunction in diaphragm muscle will allow more focused and targeted interventions designed to improve the morbidity of critically ill patients. MicroRNAs—a small class of non-coding RNAs about 22 nucleotides long, and the microRNA regulatory network plays a significant role in skeletal muscle mitochondrial regulation, differentiation, proliferation, and apoptosis. A rodent cecal-ligation and puncture (CLP) model was used to mimic sepsis-induced critical illness. The CLP model involved ligation of 50% of the cecum below the ileocecal valve in adult C57BL6 mice, followed by needle puncture of the cecum resulting in mid-grade sepsis. Mice survived for 48 hours or more, following injury. The diaphragm muscle was harvested from adult mice 48 hours following CLP (N=6) or a sham CLP procedure (N=6). Our primary finding was moderate grade CLP increases expression of mitochondria associated microRNA in the diaphragm. Correspondingly, genes associated with mitochondrial biogenesis decreased. Our study provides evidence for sepsis mediated dysregulation of mitochondrial homeostasis. This may play a role in diaphragm muscle dysfunction, respiratory failure, and difficult weaning from mechanical ventilation in critically ill patients.