Petrosyan Mikael, Guner Yigit S, Williams Monica, Grishin Anatoly, Ford Henri R
Childrens Hospital Los Angeles, Keck School of Medicine, University of Southern California, 4650 Sunset Blvd, Mailstop #72, Los Angeles, CA 90027, USA.
Pediatr Surg Int. 2009 Apr;25(4):309-18. doi: 10.1007/s00383-009-2344-8. Epub 2009 Mar 20.
Necrotizing enterocolitis (NEC) is a devastating disease that predominantly affects premature neonates. The mortality associated with NEC has not changed appreciably over the past several decades. The underlying etiology of NEC remains elusive, although bacterial colonization of the gut, formula feeding, and perinatal stress have been implicated as putative risk factors. The disease is characterized by massive epithelial destruction, which results in gut barrier failure. The exact molecular and cellular mechanisms involved in this complex disease are poorly understood. Recent studies have provided significant insight into our understanding of the pathogenesis of NEC. Endogenous mediators such as prostanoids, cyclooxygenases, and nitric oxide may play a role in the development of gut barrier failure. Understanding the structural architecture of the gut barrier and the cellular mechanisms that are responsible for gut epithelial damage could lead to the development of novel diagnostic, prophylactic and therapeutic strategies in NEC.
坏死性小肠结肠炎（NEC）是一种主要影响早产儿的毁灭性疾病。在过去几十年中，与NEC相关的死亡率并无明显变化。尽管肠道细菌定植、配方奶喂养和围产期应激被认为是可能的危险因素，但NEC的潜在病因仍不清楚。该疾病的特征是大量上皮细胞破坏，导致肠道屏障功能衰竭。人们对这种复杂疾病所涉及的确切分子和细胞机制了解甚少。最近的研究为我们理解NEC的发病机制提供了重要见解。内源性介质如前列腺素、环氧化酶和一氧化氮可能在肠道屏障功能衰竭的发展中起作用。了解肠道屏障的结构架构以及导致肠道上皮损伤的细胞机制，可能会促成NEC新型诊断、预防和治疗策略的开发。
