Systematic review explores bile acid metabolism dysregulation and signaling in necrotizing enterocolitis pathogenesisCould a digestive chemical imbalance be harming premature babies' intestines?

This systematic review article summarizes current research progress on the role of bile acid metabolism dysregulation and signaling pathways in the pathogenesis of necrotizing enterocolitis (NEC) in premature infants. The review describes core characteristics including abnormal bile acid composition and imbalanced enterohepatic circulation, and identifies intestinal epithelial cells as central integrators and primary targets of bile acid dysregulation and intestinal microbiota dysbiosis in NEC. A bidirectional regulatory relationship between bile acids and intestinal microbiota is noted.

The review proposes that excessive activation of the Farnesoid X receptor (FXR) drives the occurrence and development of NEC through mechanisms including damage to the intestinal epithelial barrier, induction of ferroptosis in intestinal epithelial cells, and exacerbation of intestinal immune inflammation. No specific intervention, comparator, primary outcome, or quantitative results with effect sizes, absolute numbers, or statistical measures are reported, as this is a synthesis of existing research rather than an original clinical study.

Safety and tolerability data are not reported. The review explores the potential value and clinical translational prospects of novel prevention and treatment strategies targeting bile acid metabolism and signaling pathways, providing theoretical support for optimizing NEC diagnosis and treatment and improving prognosis in premature infants. Key limitations include the absence of original clinical trial data, patient-level outcomes, and quantitative effect sizes. The described mechanisms are from summarized research and are not proven in clinical intervention studies.