The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles
Top Cited Papers
Open Access
- 31 March 2012
- journal article
- review article
- Published by Oxford University Press (OUP) in Cardiovascular Research
- Vol. 95 (2), 194-204
- https://doi.org/10.1093/cvr/cvs135
Abstract
Vascular smooth muscle cells (VSMCs) are the stromal cells of the vascular wall, continually exposed to mechanical signals and biochemical components generated in the blood compartment. They are involved in all the physiological functions and the pathological changes taking place in the vascular wall. Owing to their contractile tonus, VSMCs of resistance vessels participate in the regulation of blood pressure and also in hypertension. VSMCs of conduit arteries respond to hypertension-induced increases in wall stress by an increase in cell protein synthesis (hypertrophy) and extracellular matrix secretion. These responses are mediated by complex signalling pathways, mainly involving RhoA and extracellular signal-regulated kinase1/2. Serum response factor and miRNA expression represent main mechanisms controlling the pattern of gene expression. Ageing also induces VSMC phenotypic modulation that could have influence on cell senescence and loss of plasticity and reprogramming. In the early stages of human atheroma, VSMCs support the lipid overload. Endocytosis/phagocytosis of modified low-density lipoproteins, free cholesterol, microvesicles, and apoptotic cells by VSMCs plays a major role in the progression of atheroma. Migration and proliferation of VSMCs in the intima also participate in plaque progression. The medial VSMC is the organizer of the inwardly directed angiogenic response arising from the adventitia by overexpressing vascular endothelial growth factor in response to lipid-stimulated peroxisome proliferator-activated receptor-γ, and probably also the organizer of the adventitial immune response by secreting chemokines. VSMCs are also involved in the response to proteolytic injury via their ability to activate blood-borne proteases, to secrete antiproteases, and to clear protease/antiprotease complexes.Keywords
This publication has 101 references indexed in Scilit:
- Elastin Degradation and Vascular Smooth Muscle Cell Phenotype Change Precede Cell Loss and Arterial Medial Calcification in a Uremic Mouse Model of Chronic Kidney DiseaseThe American Journal of Pathology, 2011
- Recapitulation of premature ageing with iPSCs from Hutchinson–Gilford progeria syndromeNature, 2011
- Vascular smooth muscle cell peroxisome proliferator-activated receptor-γ deletion promotes abdominal aortic aneurysmsJournal of Vascular Surgery, 2010
- NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystalsNature, 2010
- miR-145 and miR-143 regulate smooth muscle cell fate and plasticityNature, 2009
- Lymphotoxin β receptor signaling promotes tertiary lymphoid organogenesis in the aorta adventitia of aged ApoE−/− miceThe Journal of Experimental Medicine, 2009
- SRF and myocardin regulate LRP-mediated amyloid-β clearance in brain vascular cellsNature, 2008
- A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse modelProceedings of the National Academy of Sciences of the United States of America, 2008
- Tensegrity-based mechanosensing from macro to microProgress in Biophysics and Molecular Biology, 2008
- Inhibition of PDGF-BB by Factor VII-activating protease (FSAP) is neutralized by protease nexin-1, and the FSAP–inhibitor complexes are internalized via LRPBiochemical Journal, 2007