Inflammation in Atherosclerosis: From Pathophysiology to Practice

By Peter Libby, P. Ridker, G. Hansson. Journal of the American College of Cardiology, 2009

2,213 citations recorded by the source corpus.

Just three decades ago the prevailing viewpoint envisaged atherosclerosis as a bland proliferative process. (1) According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet-derived growth factor which would trigger the proliferation of smooth muscle cells in the arterial intima, and form the nidus of the atherosclerotic plaque. This cellular model of atherosclerosis updated Virchow's concepts of atherosclerosis as a response to injury formulated in the mid-nineteenth century. The advent of the cell biological era of atherosclerosis supplanted the simplistic concept of the atheroma as a passive deposition of lipid debris on the artery wall. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent work identified immune cells and mediators at work in atheromata, implicating inflammatory mechanisms in disease development. (2) The advent of gene-targeting technology enabled the testing of the roles of specific molecules in the development of experimental atherosclerosis in mice. Such data demonstrated a critical role for hypercholesterolemia and also supported the participation of immune mechanisms in the pathogenesis of atherosclerosis. (3) Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. This revolution in our thinking about the pathophysiology of atherosclerosis has begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/30cf74ac92849e17576db6f1978b3863556b436c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Peter Libby
2. P. Ridker
3. T. Thuren
4. A. Zalewski
5. G. Moneta
6. Danyang Li
7. Minghua Wu
8. G. Hansson

In Immunology

1. Peter Libby
2. P. Ridker
3. Danyang Li
4. Minghua Wu
5. G. Hansson
6. I. Tabas
7. Wenshuai Wang
8. Anna Marie Pyle

In Molecular Biology

1. Peter Libby
2. P. Ridker
3. Danyang Li
4. Minghua Wu

Citations in the corpus

• Global vascular guidelines on the management of chronic limb-threatening ischemia (2019, background): “Strategies are urgently required to improve availability and affordability of drugs so that vascular specialists can treat their patients to target.321 There have been concerns that drugs reducing heart rate and blood pressure will worsen ischemia in patients with PAD.”
• Obesity and C‐reactive protein in various populations: a systematic review and meta‐analysis (2013, background): “Recently, inflammation has been understood to be a key pathogenic mechanism in the initiation and progression of CVD (3), and great attention has been given to inflammatory markers for their ability to predict CVD risk (4).”
• Pattern recognition receptors in health and diseases (2021, background): “The formation of initial atherosclerotic plaques is caused by the interaction of macrophages and endothelial cells, macrophage infiltration, and other factors that lead to an increase in neointima.(404,405) It is worth noting that studies have shown that TLR5-mediated activation of NADPH oxidase 4 (”