Progress and challenges in translating the biology of atherosclerosis
Abstract
Atherosclerosis is a chronic disease of the arterial wall, and a leading cause of death and loss of productive life years worldwide. Research into the disease has led to many compelling hypotheses about the pathophysiology of atherosclerotic lesion formation and of complications such as myocardial infarction and stroke. Yet, despite these advances, we still lack definitive evidence to show that processes such as lipoprotein oxidation, inflammation and immunity have a crucial involvement in human atherosclerosis. Experimental atherosclerosis in animals furnishes an important research tool, but extrapolation to humans requires care. Understanding how to combine experimental and clinical science will provide further insight into atherosclerosis and could lead to new clinical applications.
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Depressive symptoms further exacerbate inflammation and contribute to the pathogenesis of various diseases of aging, many of which involve excessive cytokine activity.
“These symptoms are thought to further exacerbate inflammation and, in doing so, contribute to the pathogenesis of various diseases of aging (6–8), many of which involve excessive cytokine activity (9, 10).”
From Clustering of depression and inflammation in adolescents previously exposed to childhood adversity (2012) · cites this paper as [10]
Atherosclerosis begins with damaged endothelium that permits accumulation of oxidized LDL particles in the arterial wall, triggering an unresolved inflammatory response.
“Atherosclerosis originates from damaged endothelium that allows the accumulation of cholesterol-containing LDL particles in the arterial wall that tend to be oxidized, which triggers an inflammatory response that fails to resolve”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [144]
These limitations have motivated several groups to issue recommendations for accelerating translation of nanoparticles into the clinic.
“These limitations are among the reasons that have motivated several groups to issue recommendations for accelerating the translation of nanoparticles into the clinic158,161,162.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [162]
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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
- Nature
- Published
- 2011-05
- Volume
- 473
- Issue
- 7347
- Pages
- 317-325
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2033896075
- Semantic Scholar
- 31a83a618339a5f25357342f3633f5a423880eb6
- Cited by
- 4,010
- References
- 100
- Citations by year
- 2026: 169 · 2025: 235 · 2024: 252 · 2023: 249 · 2022: 283 · 2021: 342 · 2020: 299 · 2019: 264 · 2018: 271 · 2017: 304 · 2016: 271 · 2015: 286 · 2014: 258 · 2013: 232 · 2012: 230
- FWCI
- 22.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- atherosclerosis, atherosclerotic plaque formation, lipoprotein oxidation, inflammation, immunity, animal models, animal-to-human extrapolation, myocardial infarction, stroke, translational research
- MeSH terms
- Animals, Humans, Inflammation, Cholesterol, HDL, Cholesterol, LDL, Triglycerides, Atherosclerosis, Lipid Metabolism
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