周细胞在充血引起的狭窄后毛细血管去募集中的作用。

Current tissue microenvironment reports Pub Date : 2020-12-01 Epub Date: 2020-10-30 DOI:10.1007/s43152-020-00017-6
Sanjiv Kaul, Carmen Methner, Anusha Mishra
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引用次数: 3

摘要

目的:微血管毛细血管网络被称为周细胞的细胞包裹,周细胞是来自多个谱系的异质壁细胞群体。周细胞在机体中发挥着多方面的作用,包括血管结构和通透性、局部血流调节、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回缩中的作用,这是一种病理生理现象,在狭窄存在充血刺激并减弱充血反应后观察到。最近的发现:我们讨论了最近的观察结果,最终证明了当上游动脉狭窄存在时,周细胞是响应充血刺激收缩的细胞结构。这种反应收缩毛细血管,这可能是为了维持毛细血管静水压力,这是组织稳态的一个重要因素。尽管如此,随后充血反应的衰减可导致能量供应减少并对组织健康产生负面影响。摘要:旨在预防周细胞介导的毛细血管再募集的治疗方法可能通过减少充血血流限制而对冠状动脉狭窄和外周动脉疾病等病症有益。识别参与这种去招募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。
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The role of pericytes in hyperemia-induced capillary de-recruitment following stenosis.

Purpose: 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.

Recent findings: 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.

Summary: 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.

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