Structural Remodeling of the Extracellular Matrix in Arteriogenesis: A Review.
Structural Remodeling of the Extracellular Matrix in Arteriogenesis: A Review.
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DOI：
10.3389/fcvm.2021.761007
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发表时间：
2021
影响因子：
3.6
通讯作者：
McEnaney R
中科院分区：
文献类型：
--
作者：
Kulkarni R;Andraska E;McEnaney R
下肢动脉闭塞性疾病（AOD）导致人群的显著发病率和死亡率，高达10%的患者最终需要截肢。一种尚未完全理解的非手术血管重建的替代方法是在称为动脉生成的过程中优化身体自身的天然侧支动脉网络。在传导性血管狭窄或闭塞的情况下，导致侧支内的流量、剪切力和压力梯度增加，发生正性重塑以增加这些血管的直径和容量。通过进一步增加通过这些小动脉的流量，与仅闭塞传导血管的侧支形成相比，远端动静脉瘘（AVF）的创建将驱动增加的动脉生成，证明动脉生成形成更大、更有效的侧支的能力超过动脉闭塞后自发实现的能力。动脉依赖于由弹性纤维和胶原组成的细胞外基质（ECM），其在血液动力学应激下提供稳定性，并且ECM重塑是允许成熟动脉结构中的直径和流动传导增加所必需的。当发生正性重塑时，基质金属蛋白酶（MMPs）和其他弹性蛋白酶对板层和内弹性层（IEL）的消化导致弹性结构的重排和变薄，并且可能被无序的弹性蛋白合成所取代，而没有恢复弹性功能。这导致壁应变传递至胶原蛋白，并可能沿沿着侧支网络发生胰十二指肠动脉（PDA）变性，如在腹腔闭塞后的胰十二指肠动脉（PDA）和肠系膜下动脉（IMA）并发腹腔和上级肠系膜动脉（SMA）闭塞中所见。需要进一步了解侧枝的发育，以更好地了解动脉粥样硬化性病变和优化侧枝形成。
Lower extremity arterial occlusive disease (AOD) results in significant morbidity and mortality for the population, with up to 10% of patients ultimately requiring amputation. An alternative method for non-surgical revascularization which is yet to be fully understood is the optimization of the body's own natural collateral arterial network in a process known as arteriogenesis. Under conditions of conductance vessel stenosis or occlusion resulting in increased flow, shear forces, and pressure gradients within collaterals, positive remodeling occurs to increase the diameter and capacity of these vessels. The creation of a distal arteriovenous fistula (AVF) will drive increased arteriogenesis as compared to collateral formation with the occlusion of a conductance vessel alone by further increasing flow through these arterioles, demonstrating the capacity for arteriogenesis to form larger, more efficient collaterals beyond what is spontaneously achieved after arterial occlusion. Arteries rely on an extracellular matrix (ECM) composed of elastic fibers and collagens that provide stability under hemodynamic stress, and ECM remodeling is necessary to allow for increased diameter and flow conductance in mature arterial structures. When positive remodeling occurs, digestion of lamella and the internal elastic lamina (IEL) by matrix metalloproteinases (MMPs) and other elastases results in the rearrangement and thinning of elastic structures and may be replaced with disordered elastin synthesis without recovery of elastic function. This results in transmission of wall strain to collagen and potential for aneurysmal degeneration along collateral networks, as is seen in the pancreaticoduodenal artery (PDA) after celiac occlusion and inferior mesenteric artery (IMA) with concurrent celiac and superior mesenteric artery (SMA) occlusions. Further understanding into the development of collaterals is required to both better understand aneurysmal degeneration and optimize collateral formation in AOD.
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影响因子：
5.6
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影响因子：
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