Possible mechanical roles of glycosaminoglycans in thoracic aortic dissection and associations with dysregulated transforming growth factor-β.
Possible mechanical roles of glycosaminoglycans in thoracic aortic dissection and associations with dysregulated transforming growth factor-β.
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DOI：
10.1159/000342436
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发表时间：
2013
影响因子：
1.7
通讯作者：
Humphrey JD
中科院分区：
文献类型：
--
作者：
Humphrey JD
胸主动脉主动脉瘤和夹层(TAADs)的四个明显的组织病理学特征是弹性纤维断裂或降解、平滑肌丢失、糖胺多聚和纤维胶原重构。其中，糖胺聚糖似乎是这些病变所特有的。该综述承认转化生长因子-β(β)异常在TAADs中的重要性，并提出一个补充假说，即转化生长因子-β的增加可能有助于糖胺聚糖在近端胸主动脉中膜的积聚。无论如何，观察到的糖胺聚糖池可能会降低抗拉强度，导致应力集中，并增加椎板内膨胀压力，所有这些都可能引发局部分层，这些分层随后可能作为夹层传播，导致假腔或破裂。目前迫切需要研究糖胺多聚糖在TAADs中积累的潜在的力学和生物学后果，并阐明负责的信号通路，特别是关注非中胚层血统的合成细胞。这样的研究可以提供对夹层机制的洞察，以及一种细胞因子过度表达似乎自相矛盾的作用，这种细胞因子通常与纤维化有关，但与导致灾难性机械故障的主动脉退行性疾病有关。
Four distinguishing histopathological characteristics of thoracic aortic aneurysms and dissections (TAADs) are the fragmentation or degradation of elastic fibers, loss of smooth muscle, pooling of glycosaminoglycans, and remodeling of fibrillar collagens. Of these, pooling of glycosaminoglycans appears to be unique to these lesions. This review acknowledges the importance of dysregulated transforming growth factor–beta (TGF-β) in TAADs and offers a complementary hypothesis that increased TGF-β could contribute to the accumulation of glycosaminoglycans in the media of the proximal thoracic aorta. Regardless, observed pools of glycosaminoglycans could decrease tensile strength, cause stress concentrations, and increase intralamellar swelling pressure, all of which could initiate local delaminations that could subsequently propagate as dissections and result in a false lumen or rupture. There is a pressing need to investigate potential mechanical as well as biological consequences of accumulated glycosaminoglycans in TAADs and to elucidate responsible signaling pathways, with particular attention to synthetic cells of non-mesodermal lineage. Such research could provide insight into the mechanisms of dissection and the seemingly paradoxical role of the over-expression of a cytokine that is typically associated with fibrosis but is implicated in a degenerative disease of the aorta that can result in a catastrophic mechanical failure.
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影响因子：
3.3
作者：
Borges, Luciano F.;Touat, Ziad;Michel, Jean-Baptiste
通讯作者：
Michel, Jean-Baptiste
影响因子：
7
作者：
Bian L;Angione SL;Ng KW;Lima EG;Williams DY;Mao DQ;Ateshian GA;Hung CT
通讯作者：
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影响因子：
37.8
作者：
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通讯作者：
Allaire, E
影响因子：
3.9
作者：
Evanko, SP;Johnson, PY;Wight, TN
通讯作者：
Wight, TN
DOI：
10.1152/ajpheart.01027.2007
发表时间：
2008-03-01
影响因子：
4.8
作者：
Azeloglu, Evren U.;Albro, Michael B.;Costa, Kevin D.
通讯作者：
Costa, Kevin D.