Pediatric researchJul 25, 2026

Changing role of energy-making cell problems and their cleanup in severe intestinal tissue damage

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 26, 2026

Abstract

Mitochondrial dysfunction is central to necrotizing enterocolitis (NEC) pathogenesis.

NEC is characterized by a complex inflammatory response driven by cytokines.
Emerging evidence indicates that mitochondrial dysfunction may link microbial signals to immune responses.
This dysfunction is associated with subsequent epithelial injury in the context of NEC.
ACSL1 has been identified as a potential biomarker and therapeutic target for NEC.
Future research should focus on the timing of mitochondrial dysfunction and the role of mitophagy.

Simplified

Necrotizing enterocolitis (NEC) is a severe, multifactorial disease of prematurity characterized by a heterogeneous pathophysiology. A dysregulated cytokine-driven inflammatory response is central to its progression, underscoring the need to identify key molecular triggers and pathways. Emerging evidence suggests that mitochondrial dysfunction represents a central nidus linking microbial signals to immune responses, and ultimately to epithelial injury. Future studies defining the timing and mechanisms of mitochondrial dysfunction and the role of mitophagy to better understand the interplay of the microbiome, immune responses, and mitochondria in the pathogenesis of NEC are greatly needed. IMPACT: Mitochondrial dysfunction is central to NEC pathogenesis, linking dysbiosis, immune dysregulation, and epithelial injury, and redefining NEC as an immunometabolic disease. ACSL1 emerges as a promising biomarker and therapeutic target, with potential to guide early diagnosis and modulate inflammation and oxidative stress. Future focus on timing and mitophagy may enable early detection and targeted interventions before irreversible intestinal injury develops, improving outcomes in NEC.

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PubMed

Changing role of energy-making cell problems and their cleanup in severe intestinal tissue damage

Abstract

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