Elastic fibres and vascular structure in hypertension.
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.
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, C/ Arzobispo Morcillo 2, 28029-Madrid, Spain. Silvia.Arribas@uam.es
Silvia M
SM
Arribas
Aleksander
A
Hinek
M Carmen
MC
González
D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001808:Blood Vessels / Q000473:pathology*; D049109:Cell Proliferation; D003094:Collagen / Q000502:physiology; D004032:Diet; D004547:Elastic Tissue / Q000187:drug effects / Q000502:physiology*; D004549:Elastin / Q000096:biosynthesis / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000235:genetics; D000071837:Fibrillins; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D016023:Integrins / Q000502:physiology; D008562:Membrane Glycoproteins / Q000235:genetics; D008840:Microfilament Proteins / Q000235:genetics; D011509:Proteoglycans / Q000502:physiology
D000959:Antihypertensive Agents; D016326:Extracellular Matrix Proteins; C492373:FBLN5 protein, human; D000071837:Fibrillins; D016023:Integrins; D008562:Membrane Glycoproteins; D008840:Microfilament Proteins; D011509:Proteoglycans; C030340:elastin microfibril interface located protein; D003094:Collagen; D004549:Elastin