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The role of vascular smooth muscle cells on the pathogenesis of atherosclerosis.
Acta Med Indones. 2007 Apr-Jun; 39(2):86-93.AM

Abstract

Atherosclerosis is the leading cause of death and disability. The lesions of atherosclerosis represent a series of highly specific cellular and molecular responses. The earliest changes that precede the formation of lesions of atherosclerosis take place in the endothelium (EC), with resultant endothelial dysfunction. The EC-induced injury can result in increased lipid permeability, macrophage recruitment, formation of foam cells, and recruitment of T-lymphocytes and platelet. After intimal injury, different cell types,including ECs, platelets, and inflammatory cells release mediators, such as growth factors and cytokines that induce multiple effects including phenotype change of vascular smooth muscle cells (VSMC) from the quiescent "contractile" phenotype state to the active "synthetic" state, that can migrate and proliferate from media to the intima. The inflammatory response simulates migration and proliferation of VSMC that become intermixed with the area of inflammation to form an intermediate lesion. These responses continue uninhibited and is accompanied by accumulation of new extra cellular matrix (ECM). The migratory and proliferative activities of VSMC are regulated by growth promoters such as platelet derived growth factors (PGF), endothelin-1 (ET-1), thrombin, fibroblast growth factor (FGF), interleukin-1 (IL-1) and inhibitors such as, heparin sulfates , nitric oxide (NO), transforming growth factor (TGF)-beta. The matrix metallo proteinases (MMPs) could also participate in the process of VSMC migration. MMPs could catalyze and remove the basement membrane around VSMC and facilitate contacts with the interstitial matrix. This could promote a change from quiescent, contractile VSMC to cells capable of migrating and proliferating to mediate repair. The VSMC regulation is a very complex process, VSMC are stimulated to proliferate and migrate by some kind of cytokines, growth factors, angiotensin II (Ang-II). Together with apoptosis, proliferation and migration of VSMC are vital to the pathogenesis of atherosclerosis and plaque rupture. Rupture of the plaque is associated with increased fibrous cap macrophage, increased VSMC apoptosis, and reduced fibrous cap VSMC. VSMC are the only cells with plaques capable of synthesizing structurally important collagen isoforms, and the apoptosis of VSMC might promote plaque rupture.

Authors+Show Affiliations

Department of Internal Medicine, Faculty of Medicine, Brawijaya University, Malang.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17933075

Citation

Rudijanto, Achmad. "The Role of Vascular Smooth Muscle Cells On the Pathogenesis of Atherosclerosis." Acta Medica Indonesiana, vol. 39, no. 2, 2007, pp. 86-93.
Rudijanto A. The role of vascular smooth muscle cells on the pathogenesis of atherosclerosis. Acta Med Indones. 2007;39(2):86-93.
Rudijanto, A. (2007). The role of vascular smooth muscle cells on the pathogenesis of atherosclerosis. Acta Medica Indonesiana, 39(2), 86-93.
Rudijanto A. The Role of Vascular Smooth Muscle Cells On the Pathogenesis of Atherosclerosis. Acta Med Indones. 2007 Apr-Jun;39(2):86-93. PubMed PMID: 17933075.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of vascular smooth muscle cells on the pathogenesis of atherosclerosis. A1 - Rudijanto,Achmad, PY - 2007/10/16/pubmed PY - 2007/12/7/medline PY - 2007/10/16/entrez SP - 86 EP - 93 JF - Acta medica Indonesiana JO - Acta Med Indones VL - 39 IS - 2 N2 - Atherosclerosis is the leading cause of death and disability. The lesions of atherosclerosis represent a series of highly specific cellular and molecular responses. The earliest changes that precede the formation of lesions of atherosclerosis take place in the endothelium (EC), with resultant endothelial dysfunction. The EC-induced injury can result in increased lipid permeability, macrophage recruitment, formation of foam cells, and recruitment of T-lymphocytes and platelet. After intimal injury, different cell types,including ECs, platelets, and inflammatory cells release mediators, such as growth factors and cytokines that induce multiple effects including phenotype change of vascular smooth muscle cells (VSMC) from the quiescent "contractile" phenotype state to the active "synthetic" state, that can migrate and proliferate from media to the intima. The inflammatory response simulates migration and proliferation of VSMC that become intermixed with the area of inflammation to form an intermediate lesion. These responses continue uninhibited and is accompanied by accumulation of new extra cellular matrix (ECM). The migratory and proliferative activities of VSMC are regulated by growth promoters such as platelet derived growth factors (PGF), endothelin-1 (ET-1), thrombin, fibroblast growth factor (FGF), interleukin-1 (IL-1) and inhibitors such as, heparin sulfates , nitric oxide (NO), transforming growth factor (TGF)-beta. The matrix metallo proteinases (MMPs) could also participate in the process of VSMC migration. MMPs could catalyze and remove the basement membrane around VSMC and facilitate contacts with the interstitial matrix. This could promote a change from quiescent, contractile VSMC to cells capable of migrating and proliferating to mediate repair. The VSMC regulation is a very complex process, VSMC are stimulated to proliferate and migrate by some kind of cytokines, growth factors, angiotensin II (Ang-II). Together with apoptosis, proliferation and migration of VSMC are vital to the pathogenesis of atherosclerosis and plaque rupture. Rupture of the plaque is associated with increased fibrous cap macrophage, increased VSMC apoptosis, and reduced fibrous cap VSMC. VSMC are the only cells with plaques capable of synthesizing structurally important collagen isoforms, and the apoptosis of VSMC might promote plaque rupture. SN - 0125-9326 UR - https://www.unboundmedicine.com/medline/citation/17933075/The_role_of_vascular_smooth_muscle_cells_on_the_pathogenesis_of_atherosclerosis_ L2 - http://www.inaactamedica.org/archives/2007/17933075.pdf DB - PRIME DP - Unbound Medicine ER -