Arribas Silvia M, Hinek Aleksander, González M Carmen
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, C/ Arzobispo Morcillo 2, 28029-Madrid, Spain.
Pharmacol Ther. 2006 Sep;111(3):771-91. doi: 10.1016/j.pharmthera.2005.12.003. Epub 2006 Feb 20.
Blood vessels are dynamic structures composed of cells and extracellular matrix (ECM), which are in continuous cross-talk with each other. Thus, cellular changes in phenotype or in proliferation/death rate affect ECM synthesis. In turn, ECM elements not only provide the structural framework for vascular cells, but they also modulate cellular function through specific receptors. These ECM-cell interactions, together with neurotransmitters, hormones and the mechanical forces imposed by the heart, modulate the structural organization of the vascular wall. It is not surprising that pathological states related to alterations in the nervous, humoral or haemodynamic environment-such as hypertension-are associated with vascular wall remodeling, which, in the end, is deleterious for cardiovascular function. However, the question remains whether these structural alterations are simply a consequence of the disease or if there are early cellular or ECM alterations-determined either genetically or by environmental factors-that can predispose to vascular remodeling independent of hypertension. Elastic fibres might be key elements in the pathophysiology of hypertensive vascular remodeling. In addition to the well known effects of hypertension on elastic fibre fatigue and accelerated degradation, leading to loss of arterial wall resilience, recent investigations have highlighted new roles for individual components of elastic fibres and their degradation products. These elements can act as signal transducers and regulate cellular proliferation, migration, phenotype, and ECM degradation. In this paper, we review current knowledge regarding components of elastic fibres and discuss their possible pathomechanistic associations with vascular structural abnormalities and with hypertension development or progression.
血管是由细胞和细胞外基质（ECM）组成的动态结构，它们之间持续相互作用。因此，细胞表型或增殖/死亡率的变化会影响ECM的合成。反过来，ECM成分不仅为血管细胞提供结构框架，还通过特定受体调节细胞功能。这些ECM与细胞的相互作用，连同神经递质、激素以及心脏施加的机械力，调节血管壁的结构组织。毫不奇怪，与神经、体液或血液动力学环境改变相关的病理状态——如高血压——与血管壁重塑有关，而这最终对心血管功能有害。然而，问题仍然存在，即这些结构改变仅仅是疾病的结果，还是存在早期的细胞或ECM改变——由遗传或环境因素决定——可能导致独立于高血压的血管重塑。弹性纤维可能是高血压血管重塑病理生理学中的关键因素。除了高血压对弹性纤维疲劳和加速降解的众所周知的影响，导致动脉壁弹性丧失外，最近的研究突出了弹性纤维单个成分及其降解产物的新作用。这些成分可以作为信号转导分子，调节细胞增殖、迁移、表型和ECM降解。在本文中，我们综述了关于弹性纤维成分的现有知识，并讨论它们与血管结构异常以及高血压发生或进展可能的病理机制关联。
