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Molecular Biology of Atherosclerosis
Abstract
At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-α and related family members leading to activation of NF-κB; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.
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Tissue-Specific Roles of ABCA1 Influence Susceptibility to Atherosclerosis
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LXRα Regulates Macrophage Arginase 1 Through PU.1 and Interferon Regulatory Factor 8
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Metadata
- Authors
- Hopkins, P. N.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2013-07
- Volume
- 93
- Issue
- 3
- Pages
- 1317-1542
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2004475371
- Cited by
- 459
- References
- 176
- FWCI
- 2.30
- Type
- journal article
- Language
- en
- Open access
- closed
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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