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[动脉粥样硬化形成与免疫炎症]

[Atherogenesis and immune inflammation].

作者信息

Nagornev V A

出版信息

Arkh Patol. 1995 May-Jun;57(3):6-14.

PMID:7677585
Abstract

A universal approach to atherosclerosis pathogenesis is discussed according to which humoral factors, first of all modified lipoproteins and cells of the vascular wall, are considered as an entity. Although the arterial wall is estimated as a target organ realizing leading pathogenetic factors, the process in the arterial wall is a trigger of cell reactions resulting in the formation of an atherosclerotic plaque. Immune inflammation developing in the vascular wall as a response to deposition or formation of the autoimmune complex that includes a modified lipoprotein as an antigen, is regarded as an integral part of atherogenesis. Cytokines produced by the activated macrophages and lymphocytes purposefully affect parietal cells promoting the formation of foam cells and phenotypic modification of GMK with their production of the components of the connective tissue matrix.

摘要

本文讨论了一种关于动脉粥样硬化发病机制的通用方法,根据该方法,体液因素,首先是修饰的脂蛋白和血管壁细胞,被视为一个整体。尽管动脉壁被认为是实现主要致病因素的靶器官,但动脉壁中的过程是细胞反应的触发因素,导致动脉粥样硬化斑块的形成。血管壁中发生的免疫炎症是对包含修饰脂蛋白作为抗原的自身免疫复合物沉积或形成的反应,被视为动脉粥样硬化发生的一个组成部分。活化的巨噬细胞和淋巴细胞产生的细胞因子有目的地影响壁细胞,促进泡沫细胞的形成以及GMK的表型改变,并使其产生结缔组织基质成分。

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