Microstructural Characterization of Resistance Artery Remodelling in Diabetes Mellitus.

Microstructural Characterization of Resistance Artery Remodelling in Diabetes Mellitus.
复制标题

糖尿病阻力动脉重塑的微观结构特征。

DOI:
10.1159/000517856
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发表时间:
2022
影响因子:
1.7
通讯作者:
Bell JS
Bell JS
中科院分区:
医学4区
文献类型:
--
作者:
Bell JS

文献摘要

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微血管重构是心血管疾病的一种症状。尽管机械环境被认为是重塑过程的主要贡献者,但目前对它的理解还很初级。目的对健康人与糖尿病人血管阻力进行形态学和力学评价。方法采用双光子荧光和二次谐波成像技术对腹部脂肪活检的人皮下阻力动脉细胞和细胞外基质在不同的跨壁压力下进行成像。研究结果为双层力学模型提供了依据。结果糖尿病抵抗动脉壁面积随血压升高而减小。这要归功于支撑外壁的厚而直的胶原纤维束的存在。异常的机械环境导致内部弹性层和内皮血管平滑肌细胞排列扭曲。结论:糖尿病微血管重构可能是应力驱动的,至少包括两个阶段:(1)外支架纤维的铺设,限制了向外扩张;(2)介质中额外胶原的沉积,可能是由于机械环境的显著改变。这项工作代表了向阐明细胞局部应激环境迈出的一步,这对于建立准确的疾病机械转导模型至关重要。
IntroductionMicrovascular remodelling is a symptom of cardiovascular disease. Despite the mechanical environment being recognized as a major contributor to the remodelling process, it is currently only understood in a rudimentary way.ObjectiveA morphological and mechanical evaluation of the resistance vasculature in health and diabetes mellitus.MethodsThe cells and extracellular matrix of human subcutaneous resistance arteries from abdominal fat biopsies were imaged using two-photon fluorescence and second harmonic generation at varying transmural pressure. The results informed a two-layer mechanical model.ResultsDiabetic resistance arteries reduced in wall area as pressure was increased. This was attributed to the presence of thick, straight collagen fibre bundles that braced the outer wall. The abnormal mechanical environment caused the internal elastic lamina and endothelial and vascular smooth muscle cell arrangements to twist.ConclusionsOur results suggest diabetic microvascular remodelling is likely to be stress-driven, comprising at least 2 stages:(1) Laying down of adventitial bracing fibres that limit outward distension, and (2) Deposition of additional collagen in the media, likely due to the significantly altered mechanical environment. This work represents a step towards elucidating the local stress environment of cells, which is crucial to build accurate models of mechanotransduction in disease.