The role of pericytes in hyperemia-induced capillary de-recruitment following stenosis.
The role of pericytes in hyperemia-induced capillary de-recruitment following stenosis.
复制标题
DOI：
10.1007/s43152-020-00017-6
复制
发表时间：
2020-12
期刊：
影响因子：
--
通讯作者：
Mishra A
中科院分区：
文献类型：
--
作者：
Kaul S;Methner C;Mishra A
微血管毛细血管网络被称为周细胞的细胞所包裹，周细胞是来自多个谱系的异质壁细胞群体。周细胞在体内发挥着多方面的作用，包括调节血管结构和通透性，调节局部血流，免疫和伤口愈合功能，诱导血管生成，以及各种祖细胞的生成。在这里，我们考虑周细胞在毛细血管去募集中的作用，这是一种病理生理现象，在狭窄存在的充血刺激后观察到，并减弱充血反应。我们讨论了最近的观察结果，最终证明周细胞是当上游动脉狭窄时，对充血刺激做出反应而收缩的细胞结构。这种反应会收缩毛细血管，这可能是为了维持毛细血管的流体静压，这是组织动态平衡的一个重要因素。然而，随之而来的充血反应的减弱可能导致能量供应的减少，并对组织健康产生负面影响。旨在防止周细胞介导的毛细血管去募集的治疗方法可能被证明在冠状动脉狭窄和外周动脉疾病等情况下是有益的，因为它减少了对充血血流的限制。识别参与这一去募集的周细胞亚型和调节这一过程的潜在分子机制将极大地有助于这一目的。
The microvascular capillary network is ensheathed by cells called pericytes - a heterogeneous population of mural cells derived from multiple lineages. Pericytes play a multifaceted role in the body, including in vascular structure and permeability, regulation of local blood flow, immune and wound healing functions, induction of angiogenesis, and generation of various progenitor cells. Here, we consider the role of pericytes in capillary de-recruitment, a pathophysiologic phenomenon that is observed following hyperemic stimuli in the presence of a stenosis and attenuates the hyperemic response. We discuss recent observations that conclusively demonstrate pericytes to be the cellular structures that contract in response to hyperemic stimuli when an upstream arterial stenosis is present. This response constricts capillaries, which is likely aimed at maintaining capillary hydrostatic pressure, an important factor in tissue homeostasis. Nonetheless, the ensuing attenuation of the hyperemic response can lead to a decrease in energy supply and negatively impact tissue health. Therapeutics aimed at preventing pericyte-mediated capillary de-recruitment may prove beneficial in conditions such as coronary stenosis and peripheral arterial disease by reducing restriction in hyperemic flow. Identification of the pericyte subtypes involved in this de-recruitment and the underlying molecular mechanisms regulating this process will greatly assist this purpose.