Suppr超能文献

小气道中的脂肪组织:多少才算足够引起功能变化?

Adipose tissue in the small airways: How much is enough to drive functional changes?

机构信息

Department of Mathematics, University of Auckland, Auckland, 1142, New Zealand.

School of Human Sciences, The University of Western Australia, Crawley, 6009, Western Australia, Australia.

出版信息

J Theor Biol. 2024 Jul 7;588:111835. doi: 10.1016/j.jtbi.2024.111835. Epub 2024 Apr 20.

Abstract

Obesity is a contributing factor to asthma severity; while it has long been understood that obesity is related to greater asthma burden, the mechanisms though which this occurs have not been fully elucidated. One common explanation is that obesity mechanically reduces lung volume through accumulation of adipose tissue external to the thoracic cavity. However, it has been recently demonstrated that there is substantial adipose tissue within the airway wall itself, and that the presence of adipose tissue within the airway wall is related to body mass index. This suggests the possibility of an additional mechanism by which obesity may worsen asthma, namely by altering the behaviour of the airways themselves. To this end, we modify Anafi & Wilson's classic model of the bistable terminal airway to incorporate adipose tissue within the airway wall in order to answer the question of how much adipose tissue would be required in order to drive substantive functional changes. This analysis suggests that adipose tissue within the airway wall on the order of 1%-2% of total airway cross-sectional area could be sufficient to drive meaningful changes, and further that these changes may interact with volume effects to magnify the overall burden.

摘要

肥胖是哮喘严重程度的一个促成因素;虽然长期以来人们都知道肥胖与更大的哮喘负担有关,但导致这种情况发生的机制尚未完全阐明。一个常见的解释是,肥胖通过胸腔外脂肪组织的积累而在机械上降低了肺容量。然而,最近已经证明,气道壁本身内部有大量的脂肪组织,并且气道壁内的脂肪组织与体重指数有关。这表明肥胖可能通过改变气道本身的行为来加重哮喘的另一种可能性。为此,我们修改了 Anafi 和 Wilson 的经典双稳态终末气道模型,在气道壁内纳入脂肪组织,以回答需要多少脂肪组织才能引起实质性功能变化的问题。这项分析表明,气道壁内的脂肪组织占总气道横截面积的 1%-2%左右,就足以引起有意义的变化,而且这些变化可能与体积效应相互作用,从而放大整体负担。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验