Ameis Dustin, Khoshgoo Naghmeh, Keijzer Richard
Department of Surgery, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada; Biology of Breathing Theme, The Children׳s Hospital Research Institute of Manitoba, Winnipeg, Manitoba, Canada.
Department of Surgery, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, Manitoba, Canada; Biology of Breathing Theme, The Children׳s Hospital Research Institute of Manitoba, Winnipeg, Manitoba, Canada.
Semin Pediatr Surg. 2017 Jun;26(3):123-128. doi: 10.1053/j.sempedsurg.2017.04.011. Epub 2017 Apr 25.
The outcomes of patients diagnosed with congenital diaphragmatic hernia (CDH) have recently improved. However, mortality and morbidity remain high, and this is primarily caused by the abnormal lung development resulting in pulmonary hypoplasia and persistent pulmonary hypertension. The pathogenesis of CDH is poorly understood, despite the identification of certain candidate genes disrupting normal diaphragm and lung morphogenesis in animal models of CDH. Defects within the lung mesenchyme and interstitium contribute to disturbed distal lung development. Frequently, a disturbance in the development of the pleuroperitoneal folds (PPFs) leads to the incomplete formation of the diaphragm and subsequent herniation. Most candidate genes identified in animal models have so far revealed relatively few strong associations in human CDH cases. CDH is likely a highly polygenic disease, and future studies will need to reconcile how disturbances in the expression of multiple genes cause the disease. Herein, we summarize the available literature on abnormal lung development associated with CDH.
先天性膈疝(CDH)患者的治疗结果最近有所改善。然而,死亡率和发病率仍然很高,这主要是由异常的肺发育导致肺发育不全和持续性肺动脉高压引起的。尽管在CDH动物模型中已经鉴定出某些破坏正常膈肌和肺形态发生的候选基因,但CDH的发病机制仍知之甚少。肺间充质和间质内的缺陷会导致远端肺发育紊乱。通常,胸膜腹膜皱襞(PPF)发育的紊乱会导致膈肌形成不完全并随后发生疝。到目前为止,在动物模型中鉴定出的大多数候选基因在人类CDH病例中显示出相对较少的强关联。CDH可能是一种高度多基因疾病,未来的研究需要阐明多个基因表达的紊乱是如何导致该疾病的。在此,我们总结了与CDH相关的异常肺发育的现有文献。