Hypoxia and Local Inflammation in Pulmonary Artery Structure and Function.
Hypoxia and Local Inflammation in Pulmonary Artery Structure and Function.
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DOI：
10.1007/978-3-319-63245-2_20
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发表时间：
2017
影响因子：
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通讯作者：
M. Thompson;R. D. Britt;C. Pabelick;Y. Prakash
中科院分区：
文献类型：
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作者：
M. Thompson;R. D. Britt;C. Pabelick;Y. Prakash
缺氧被认为是肺动脉高压等肺血管疾病的一个诱因。缺氧诱导的炎症变化可以增强ph背景下肺动脉（PA）的结构和功能变化。因此，了解肺动脉结构和功能背景下缺氧和炎症之间的联系可能与ph新疗法的开发有关。在这方面，胸腺基质淋巴生成素（TSLP），一种炎症细胞因子，脑源性神经营养因子（BDNF），一种神经营养因子，已被发现对非血管系统如气道和哮喘至关重要。虽然TSLP通常会影响免疫系统，但在非血管系统中，已经注意到非典型效应，如改变[Ca2+]岛细胞增殖：与PA相关的方面，目前几乎没有数据。同样，在神经系统中，越来越多的证据表明BDNF是由气道结构细胞局部产生的，并可能参与哮喘病理生理。在本章中，我们总结了诸如TSLP和BDNF等因素与PA的潜在相关性，以及缺氧对ph发展的影响。我们重点关注细胞来源和靶点，如PA内皮细胞（PAECs）和平滑肌细胞（PASMCs），以及TSLP或BDNF对细胞内Ca2+对血管收缩剂的反应、细胞增殖和潜在的信号级联反应的影响。
Hypoxia is recognized as a contributor to pulmonary vascular diseases such as pulmonary hypertension. Hypoxia-induced inflammatory changes can enhance structural and functional changes in pulmonary artery (PA) in the context of PH. Accordingly, understanding how hypoxia and inflammation are linked in the context of pulmonary artery structure and function could be relevant towards development of novel therapies for PH. In this regard, factors such as thymic stromal lymphopoietin (TSLP), an inflammatory cytokine, and brain-derived neurotrophic factor (BDNF), a neurotrophin, have been found critical for nonvascular systems such as airway and asthma. While TSLP canonically affects the immune system, in nonvascular systems, noncanonical effects such as altered [Ca2+]iand cell proliferation have been noted: aspects also relevant to the PA, where there is currently little to no data. Similarly, better known in the nervous system, there is increasing evidence that BDNF is locally produced by structural cells of the airway and can contribute to asthma pathophysiology. In this chapter, we summarize the potential relevance of factors such as TSLP and BDNF to the PA and in the context of hypoxia influences towards development of PH. We focus on cell sources and targets such as PA endothelial cells (PAECs) and smooth muscle cells (PASMCs), and the effects of TSLP or BDNF on intracellular Ca2+responses to vasoconstrictor agonist, cell proliferation, and potential signaling cascades involved.