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Inflammation and cardiovascular disease: From mechanisms to therapeutics
Open accessAbstract
Inflammation constitutes a complex, highly conserved cascade of molecular and cellular events. Inflammation has been labeled as "the fire within," is highly regulated, and is critical to host defense and tissue repair. In general, inflammation is beneficial and has evolved to promote survival. However, inflammation can also be maladaptive when chronically activated and sustained, leading to progressive tissue injury and reduced survival. Examples of a maladaptive response include rheumatologic disease and atherosclerosis. Despite evidence gathered by Virchow over 100 years ago showing that inflammatory white cells play a role in atherogenesis, atherosclerosis was until recently viewed as a disease of passive cholesterol accumulation in the subendothelial space. This view has been supplanted by considerable basic scientific and clinical evidence demonstrating that every step of atherogenesis, from the development of endothelial cell dysfunction to foam cell formation, plaque formation and progression, and ultimately plaque rupture stemming from architectural instability, is driven by the cytokines, interleukins, and cellular constituents of the inflammatory response. Herein we provide an overview of the role of inflammation in atherosclerotic cardiovascular disease, discuss the predictive value of various biomarkers involved in inflammation, and summarize recent clinical trials that evaluated the capacity of various pharmacologic interventions to attenuate the intensity of inflammation and impact risk for acute cardiovascular events.
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“Among these, inflammation plays a central role by contributing to insulin resistance, endothelial dysfunction, lipid accumulation, and vascular injury, thereby accelerating disease progression [36,37].”
From Navigating the potential of algal peptides: health effects, market applications, and scientific challenges (2026) · cites this paper as [37]
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Metadata
- Authors
- Alfaddagh, A., Martin, S. S., Leucker, T. M., Michos, E. D., Blaha, M. J., Lowenstein, C. J., Jones, S. R., & Toth, P. P.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Toth, Peter P.
- ORCID
- Venue
- American Journal of Preventive Cardiology
- Publisher
- Elsevier BV
- Published
- 2020-12
- Volume
- 4
- Pages
- 100130
- ISSN
- 2666-6677 (ISSN-L)
- PMC
- PMC8315628
- OpenAlex
- W3109720983
- Cited by
- 473
- References
- 239
- Citations by year
- 2026: 94 · 2025: 137 · 2024: 98 · 2023: 75 · 2022: 49 · 2021: 20
- FWCI
- 3.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- American Journal of Preventive Cardiology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Oncology › Inflammatory Biomarkers in Disease Prognosis
- Keywords
- inflammation, atherosclerosis, atherogenesis, cardiovascular disease, chronic inflammation, endothelial dysfunction, foam cell formation, plaque rupture, cytokines, interleukins, inflammatory markers, anti-inflammatory therapy, acute cardiovascular events, plaque vulnerability
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