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Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms.
Innate Immun. 2008 Apr; 14(2):63-87.II

Abstract

Cardiovascular diseases are the human diseases with the highest death rate and atherosclerosis is one of the major underlying causes of cardiovascular diseases. Inflammatory and innate immune mechanisms, employing monocytes, innate receptors, innate cytokines, or chemokines are suggested to be involved in atherogenesis. Among the inflammatory pathways the cytokines are central players. Plasma levels of cytokines and related proteins, such as CRP, have been investigated in cardiovascular patients, tissue mRNA expression was analyzed and correlations to vascular diseases established. Consistent with these findings the generation of cytokine-deficient animals has provided direct evidence for a role of cytokines in atherosclerosis. In vitro cell culture experiments further support the suggestion that cytokines and other innate mechanisms contribute to atherogenesis. Among the initiation pathways of atherogenesis are innate mechanisms, such as toll-like-receptors (TLRs), including the endotoxin receptor TLR4. On the other hand, innate cytokines, such as IL-1 or TNF, or even autoimmune triggers may activate the cells. Cytokines potently activate multiple functions relevant to maintain or spoil homeostasis within the vessel wall. Vascular cells, not least smooth muscle cells, can actively contribute to the inflammatory cytokine-dependent network in the blood vessel wall by: (i) production of cytokines; (ii) response to these potent cell activators; and (iii) cytokine-mediated interaction with invading cells, such as monocytes, T-cells, or mast cells. Activation of these pathways results in accumulation of cells and increased LDL- and ECM-deposition which may serve as an 'immunovascular memory' resulting in an ever-growing response to subsequent invasions. Thus, vascular cells may potently contribute to the inflammatory pathways involved in development and acceleration of atherosclerosis.

Authors+Show Affiliations

Martin-Luther-Universität Halle-Wittenberg, Universitätsklinik und Poliklinik für Innere Medizin , Halle (Saale), Germany. Harald.Loppnow@medizin.uniNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

18713724

Citation

Loppnow, Harald, et al. "Vascular Cells Contribute to Atherosclerosis By Cytokine- and Innate-immunity-related Inflammatory Mechanisms." Innate Immunity, vol. 14, no. 2, 2008, pp. 63-87.
Loppnow H, Werdan K, Buerke M. Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms. Innate Immun. 2008;14(2):63-87.
Loppnow, H., Werdan, K., & Buerke, M. (2008). Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms. Innate Immunity, 14(2), 63-87. https://doi.org/10.1177/1753425908091246
Loppnow H, Werdan K, Buerke M. Vascular Cells Contribute to Atherosclerosis By Cytokine- and Innate-immunity-related Inflammatory Mechanisms. Innate Immun. 2008;14(2):63-87. PubMed PMID: 18713724.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms. AU - Loppnow,Harald, AU - Werdan,Karl, AU - Buerke,Michael, PY - 2008/8/21/pubmed PY - 2008/9/27/medline PY - 2008/8/21/entrez SP - 63 EP - 87 JF - Innate immunity JO - Innate Immun VL - 14 IS - 2 N2 - Cardiovascular diseases are the human diseases with the highest death rate and atherosclerosis is one of the major underlying causes of cardiovascular diseases. Inflammatory and innate immune mechanisms, employing monocytes, innate receptors, innate cytokines, or chemokines are suggested to be involved in atherogenesis. Among the inflammatory pathways the cytokines are central players. Plasma levels of cytokines and related proteins, such as CRP, have been investigated in cardiovascular patients, tissue mRNA expression was analyzed and correlations to vascular diseases established. Consistent with these findings the generation of cytokine-deficient animals has provided direct evidence for a role of cytokines in atherosclerosis. In vitro cell culture experiments further support the suggestion that cytokines and other innate mechanisms contribute to atherogenesis. Among the initiation pathways of atherogenesis are innate mechanisms, such as toll-like-receptors (TLRs), including the endotoxin receptor TLR4. On the other hand, innate cytokines, such as IL-1 or TNF, or even autoimmune triggers may activate the cells. Cytokines potently activate multiple functions relevant to maintain or spoil homeostasis within the vessel wall. Vascular cells, not least smooth muscle cells, can actively contribute to the inflammatory cytokine-dependent network in the blood vessel wall by: (i) production of cytokines; (ii) response to these potent cell activators; and (iii) cytokine-mediated interaction with invading cells, such as monocytes, T-cells, or mast cells. Activation of these pathways results in accumulation of cells and increased LDL- and ECM-deposition which may serve as an 'immunovascular memory' resulting in an ever-growing response to subsequent invasions. Thus, vascular cells may potently contribute to the inflammatory pathways involved in development and acceleration of atherosclerosis. SN - 1753-4259 UR - https://www.unboundmedicine.com/medline/citation/18713724/Vascular_cells_contribute_to_atherosclerosis_by_cytokine__and_innate_immunity_related_inflammatory_mechanisms_ L2 - https://journals.sagepub.com/doi/10.1177/1753425908091246?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -