The ECM (extracellular matrix) is a major component of the vascular microenvironment that modulates vascular homeostasis. ECM proteins include collagens, elastin, noncollagen glycoproteins, and proteoglycans/glycosaminoglycans. ECM proteins form complex matrix structures, such as the basal lamina and collagen and elastin fibers, through direct interactions or lysyl oxidase-mediated cross-linking. Moreover, ECM proteins directly interact with cell surface receptors or extracellular secreted molecules, exerting matricellular and matricrine modulation, respectively. In addition, extracellular proteases degrade or cleave matrix proteins, thereby contributing to ECM turnover. These interactions constitute the ECM interactome network, which is essential for maintaining vascular homeostasis and preventing pathological vascular remodeling. The current review mainly focuses on endogenous matrix proteins in blood vessels and discusses the interaction of these matrix proteins with other ECM proteins, cell surface receptors, cytokines, complement and coagulation factors, and their potential roles in maintaining vascular homeostasis and preventing pathological remodeling.

中文翻译：

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细胞外基质相互作用组在调节血管稳态和重塑中的作用

ECM（细胞外基质）是调节血管稳态的血管微环境的主要组成部分。 ECM 蛋白包括胶原蛋白、弹性蛋白、非胶原糖蛋白和蛋白聚糖/糖胺聚糖。 ECM 蛋白通过直接相互作用或赖氨酰氧化酶介导的交联形成复杂的基质结构，例如基底层、胶原蛋白和弹性蛋白纤维。此外，ECM蛋白直接与细胞表面受体或细胞外分泌分子相互作用，分别发挥基质细胞和基质调节作用。此外，细胞外蛋白酶降解或切割基质蛋白，从而促进 ECM 周转。这些相互作用构成了 ECM 相互作用组网络，对于维持血管稳态和防止病理性血管重塑至关重要。本综述主要关注血管内源性基质蛋白，讨论这些基质蛋白与其他ECM蛋白、细胞表面受体、细胞因子、补体和凝血因子的相互作用，及其在维持血管稳态和预防病理重塑中的潜在作用。