Related Experiment Video
Updated: Aug 6, 2026
06:51
Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
Published on: July 28, 2023
Evolving role of mitochondrial dysfunction and mitophagy in necrotizing enterocolitis
Srinivasan Mani1, Jeffrey Shenberger2, Parvesh Mohan Garg3
1Department of Pediatrics, Division of Neonatology, University at Buffalo, Buffalo, NY, USA.
Pediatric Research
|July 25, 2026
Summary
Mitochondrial dysfunction is key in necrotizing enterocolitis (NEC), linking gut bacteria, immune issues, and injury. ACSL1 may help diagnose and treat this immunometabolic disease in premature infants.
Area of Science:
- Neonatal research
- Immunometabolism
- Gastroenterology
Background:
- Necrotizing enterocolitis (NEC) is a severe disease in premature infants.
- Inflammation and immune dysregulation are central to NEC pathogenesis.
- Mitochondrial dysfunction is increasingly recognized as a key factor.
Purpose of the Study:
- To elucidate the role of mitochondrial dysfunction in NEC.
- To identify molecular pathways linking microbial signals to epithelial injury.
- To explore ACSL1 as a potential biomarker and therapeutic target.
Main Methods:
- The study reviews emerging evidence on mitochondrial dysfunction in NEC.
- It discusses the interplay between the microbiome, immune responses, and mitochondria.
- It highlights the potential role of mitophagy.
Main Results:
- Mitochondrial dysfunction is central to NEC, linking dysbiosis, immune dysregulation, and epithelial injury.
- NEC can be redefined as an immunometabolic disease.
- ACSL1 shows promise as a biomarker and therapeutic target for modulating inflammation and oxidative stress.
Conclusions:
- Understanding mitochondrial dysfunction and mitophagy is crucial for NEC research.
- Targeting ACSL1 may offer new diagnostic and therapeutic strategies.
- This research redefines NEC as an immunometabolic condition, paving the way for novel interventions.
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