The influence of dysfunctional signaling and lipid homeostasis in mediating the inflammatory responses during atherosclerosis

Buckley, Melanie and Ramji, Dipak Purshottam ORCID: https://orcid.org/0000-0002-6419-5578 2015. The influence of dysfunctional signaling and lipid homeostasis in mediating the inflammatory responses during atherosclerosis. Biochimica et Biophysica Acta - Molecular Basis of Disease 1852 (7) , pp. 1498-1510. 10.1016/j.bbadis.2015.04.011

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Abstract

Atherosclerosis, the underlying cause of myocardial infarction and thrombotic cerebrovascular events, is responsible for the majority of deaths in westernized societies. Mortality from this disease is also increasing at a marked rate in developing countries due to the acquisition of a westernized lifestyle accompanied with elevated rates of obesity and diabetes. Atherosclerosis is recognized as a chronic inflammatory disorder associated with lipid accumulation and the development of fibrotic plaques within the walls of medium and large arteries. A range of immune cells, such as macrophages and T-lymphocytes, through the action of various cytokines, such as interleukins-1 and -33, transforming growth factor-β and interferon-γ, orchestrates the inflammatory response in this disease. The disease is also characterized by marked dysfunction in lipid homeostasis and signaling pathways that control the inflammatory response. This review will discuss the molecular basis of atherosclerosis with particular emphasis on the roles of the immune cells and cytokines along with the dysfunctional lipid homeostasis and cell signaling associated with this disease.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Subjects:	Q Science > QR Microbiology
Uncontrolled Keywords:	Atherosclerosis; Inflammation; Lipids; Lipoproteins; Cytokines; Signaling; Immune cells
Publisher:	Elsevier
ISSN:	0925-4439
Funders:	MRC
Date of First Compliant Deposit:	30 March 2016
Date of Acceptance:	8 April 2015
Last Modified:	04 May 2023 19:26
URI:	https://orca.cardiff.ac.uk/id/eprint/72778

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