Vascular Mediators in Chronic Lung Disease of Infancy: Role of Endothelial Monocyte Activating Polypeptide II ( EMAP II)

Vascular Mediators in Chronic Lung Disease of Infancy: Role of Endothelial Monocyte Activating Polypeptide II ( EMAP II)
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DOI:
10.1002/bdra.23234
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发表时间:
2014-03-01
影响因子:
--
通讯作者:
Schwarz, Margaret A.
Schwarz, Margaret A.
中科院分区:
医学4区
文献类型:
--
作者:
Lal, Charitharth Vivek;Schwarz, Margaret A.

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支气管肺发育不良(BPD)是一种早产儿慢性肺部疾病。多年来,BPD表型已经演变,但尽管新生儿管理方法取得了各种进展,但BPD负担的减少微乎其微。随着表面活性剂、糖皮质激素和新的通气策略的出现,BPD已从结构损伤疾病演变为一种新的BPD,其特征是极早产儿肺部肺泡生长停滞。这种肺泡生长不足与肺血管减少有关。一些研究者已经描述了上皮/血管的相互依赖性和血管形成、肺泡形成和肺发育不良之间的串扰的重要作用;因此,鉴定和研究调节肺血管出现和炎症的因素对于设计针对这种使人衰弱的病症的有效治疗方法变得至关重要。有效的抗血管生成和促炎蛋白内皮单核细胞激活多肽II(EMAP II)已被描述为肺血管和肺泡形成的介质,并且其表达与发育中的肺中的血管化和肺泡化的时期负相关。因此,EMAP II的研究可能在研究和设计适当的治疗方法用于异常肺发育的疾病(如BPD)中发挥重要作用。在此,我们回顾了血管对肺发育的贡献,以及血管介质如EMAP II在肺泡形成的脆弱阶段远端肺形成中的意义。出生缺陷研究(A部分)100:180-188,2014年。(c)2014 Wiley Periodicals,Inc.
Bronchopulmonary dysplasia (BPD) is a chronic lung disease of prematurity. Over the years, the BPD phenotype has evolved, but despite various advances in neonatal management approaches, the reduction in the BPD burden is minimal. With the advent of surfactant, glucocorticoids, and new ventilation strategies, BPD has evolved from a disease of structural injury into a new BPD, marked by an arrest in alveolar growth in the lungs of extremely premature infants. This deficient alveolar growth has been associated with a diminution of pulmonary vasculature. Several investigators have described the epithelial / vascular co-dependency and the significant role of crosstalk between vessel formation, alveologenesis, and lung dysplasia's; hence identification and study of factors that regulate pulmonary vascular emergence and inflammation has become crucial in devising effective therapeutic approaches for this debilitating condition. The potent antiangiogenic and proinflammatory protein Endothelial Monocyte Activating Polypeptide II (EMAP II) has been described as a mediator of pulmonary vascular and alveolar formation and its expression is inversely related to the periods of vascularization and alveolarization in the developing lung. Hence the study of EMAP II could play a vital role in studying and devising appropriate therapeutics for diseases of aberrant lung development, such as BPD. Herein, we review the vascular contribution to lung development and the implications that vascular mediators such as EMAP II have in distal lung formation during the vulnerable stage of alveolar genesis. Birth Defects Research (Part A) 100:180-188, 2014. (c) 2014 Wiley Periodicals, Inc.