Vascular Remodeling in Pulmonary Arterial Hypertension: The Potential Involvement of Innate and Adaptive Immunity.
Vascular Remodeling in Pulmonary Arterial Hypertension: The Potential Involvement of Innate and Adaptive Immunity.
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DOI：
10.3389/fmed.2021.806899
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发表时间：
2021
影响因子：
3.9
通讯作者：
van Paassen P
中科院分区：
文献类型：
--
作者：
Tobal R;Potjewijd J;van Empel VPM;Ysermans R;Schurgers LJ;Reutelingsperger CP;Damoiseaux JGMC;van Paassen P
肺动脉高压(PAH)是一种发病率高、病死率高的危重疾病。目前的治疗方法主要集中在血管扩张剂以改善预后。然而，最近的文献表明，免疫细胞和间质血管细胞之间的重要相互作用在肺血管系统的病理性改变中起着重要作用。PAH的免疫学发病机制是免疫细胞和血管基质细胞之间的复杂相互作用，通过直接接触和/或它们产生细胞因子、趋化因子和生长因子等细胞外/扩散因子。这些包括B细胞-肥大细胞轴、内皮细胞介导的成纤维细胞激活和随后的M2巨噬细胞极化、抗内皮细胞抗体和IL-6对血管细胞的多种作用。该综述旨在概述免疫机制引起的血管细胞的主要病理生理变化，导致血管重塑、肺血管阻力增加，最终导致PAH。考虑到潜在的免疫学机制，这些机制可能是阻止疾病进展的关键。
Pulmonary arterial hypertension (PAH) is a severe disease with high morbidity and mortality. Current therapies are mainly focused on vasodilative agents to improve prognosis. However, recent literature has shown the important interaction between immune cells and stromal vascular cells in the pathogenic modifications of the pulmonary vasculature. The immunological pathogenesis of PAH is known as a complex interplay between immune cells and vascular stromal cells, via direct contacts and/or their production of extra-cellular/diffusible factors such as cytokines, chemokines, and growth factors. These include, the B-cell—mast-cell axis, endothelium mediated fibroblast activation and subsequent M2 macrophage polarization, anti-endothelial cell antibodies and the versatile role of IL-6 on vascular cells. This review aims to outline the major pathophysiological changes in vascular cells caused by immunological mechanisms, leading to vascular remodeling, increased pulmonary vascular resistance and eventually PAH. Considering the underlying immunological mechanisms, these mechanisms may be key to halt progression of disease.
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