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Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.119 Figure 1 Factors that attenuate or prevent the development of NEC in experimental models Figure 1 | Factors that attenuate or prevent the development of NEC in experimental models. Activation of the innate immune receptor Toll-like receptor 4 (TLR4) plays an essential part in the development of necrotizing enterocolitis (NEC) by increasing enterocyte and intestinal stem cell apoptosis and impairing mucosal healing through decreased restitution and proliferation. These events lead to disruption of the epithelial barrier, which allows luminal bacteria to translocate and trigger a systemic inflammatory response, sepsis, multiple organ failure and death. Counter-regulatory factors can be exploited in order to dampen TLR4 signalling and expression to prevent the development of NEC. Natural factors include: epidermal growth factor (EGF)71,140,185,186, heparin-binding EGF-like growth factor (HB-EGF)186,187,188, nod-like receptor 2 (NOD2)189, Toll-like receptor 9 (TLR9)67,190 and platelet-activating factor acetylhydrolase (PAF-AH)90. Exogenous factors include: the small-molecule TLR4 inhibitor C34 (Ref. 68), bacterial (CpG) DNA67,190, muramyl dipeptide (MDP)189, sodium nitrate66, glutamine191, celastrol (also known as tripterine)192 and dibenzazepine73. EGFR, epidermal growth factor receptor; eNOS, endothelial nitric oxide synthase; Hsp70, heat shock protein 70; PAF, platelet-activating factor; SMAC, second mitochondria-derived activator of caspase (also known as Diablo homolog, mitochondrial). Niño, D. F. et al. (2016) Necrotizing enterocolitis: new insights into pathogenesis and mechanisms Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.119