Inflammation in Atherosclerosis
Open accessAbstract
Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. 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. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now 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.
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Inflammation is a critical driver of atherosclerosis and an independent risk factor for myocardial infarction and cardiovascular death.
“Inflammation is a critical driver of atherosclerosis and an independent risk factor for myocardial infarction and cardiovascular death.1”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [1]
Cellular senescence and atherosclerosis share multiple causative stimuli.
“Intriguingly, cellular senescence and atherosclerosis share multiple causative stimuli1,11,12: oxidized and electronegative low-density lipoprotein (LDL),13,14 inflammation,15 reactive oxygen species,8 cigarette smoke,16 hypertension,17 hyperglycaemia,18 cytomegalovirus (CMV) infection,19 telomere attrition,20 mitochondrial failure,21 dysfunctional autophagy,22 and genomic damage.8”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [1]
Innate and adaptive immune activation drives atherogenesis from early endothelial dysfunction to acute thrombotic complications.
“Activation of both innate and adaptive immunity actively contributes to the initiation and progression of atherogenesis, from early endothelial dysfunction to the development of acute thrombotic complications”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [147]
Rosuvastatin therapy reduces major cardiovascular events in healthy individuals without hyperlipidaemia but with elevated high-sensitivity CRP.
“statin therapy with rosuvastatin reduces the incidence of major cardiovascular events in healthy individuals who are free from hyperlipidaemia but who have elevated high-sensitivity CRP levels”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [147]
Consistent SASP elements in the majority of senescent cells are IL-1α, IL-1β, IL-6, IL-8, IL-18, and TNF-α, all of which are clinically validated CVD risk factors.
“Consistent SASP elements in the majority of senescent cells are IL-1α, IL-1β, IL-6, IL-8, IL-18, and TNF-α,15,105,110 all of which are clinically validated CVD risk factors.1,5”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [1]
Corticosteroids have anti-inflammatory effects in atherosclerosis but are not considered for long-term administration owing to poor pharmacokinetic profile and adverse side effects.
“Corticosteroids have anti-inflammatory effects in atherosclerosis, although they are not considered for long-term administration owing to a poor pharmacokinetic profile and adverse side effects79,81.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [79]
The recognition of the role of inflammation in atherosclerosis has led to the formulation of anti-inflammatory drugs tailored to atherosclerosis, several of which are currently under investigation in clinical trials.
“The recognition of the role of inflammation in atherosclerosis has led to the formulation of anti-inflammatory drugs tailored to atherosclerosis, several of which are currently under investigation in clinical trials79,80.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [79]
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- Authors
- Libby, P., Ridker, P. M., & Hansson, G. K.
- Affiliations
- Brigham and Women's Hospital (US)
- Karolinska University Hospital (SE)
- Corresponding author
- Libby, Peter
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 54
- Issue
- 23
- Pages
- 2129-2138
- ISSN
- 0735-1097 (ISSN-L)
- PMC
- PMC2834169
- OpenAlex
- W1552829599
- Cited by
- 2,228
- References
- 75
- Citations by year
- 2026: 158 · 2025: 158 · 2024: 90 · 2023: 102 · 2022: 123 · 2021: 153 · 2020: 133 · 2019: 148 · 2018: 128 · 2017: 112 · 2016: 129 · 2015: 125 · 2014: 132 · 2013: 137 · 2012: 154
- FWCI
- 10.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Fondation Leducq
- Swedish Research Council
- Swedish Heart-Lung Foundation
- Donald W. Reynolds Foundation
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cerebrovascular and Carotid Artery Diseases
- Keywords
- atherosclerosis, inflammation, atherogenesis, innate immunity, adaptive immunity, vascular smooth muscle cell proliferation, endothelial injury, platelet aggregation, atherosclerotic plaque, risk factors
- MeSH terms
- Anticholesteremic Agents, Cholesterol, Humans, Immunity, Innate, Inflammation, Muscle, Smooth, Vascular, Platelet Aggregation, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cell Proliferation, Atherosclerosis
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