Mechanisms of Resolution of Inflammation: A Focus on Cardiovascular Disease
Abstract
The inflammatory response is an integral part of the innate immune mechanism that is triggered in response to a real or perceived threat to tissue homeostasis, with a primary aim of neutralizing infectious agents and initiating repair to damaged tissue. By design, inflammation is a finite process that resolves as soon as the threat of infection abates and sufficient repair to the tissue is complete. Resolution of inflammation involves apoptosis and subsequent clearance of activated inflammatory cells – a tightly regulated event. Chronic inflammation is a characteristic feature in virtually all inflammatory diseases, including atherosclerosis, and it is becoming increasingly clear that derangement of the processes usually involved in resolution of inflammation is an underlying feature of chronic inflammatory conditions. This review will draw on evidence from a range of diseases in which dysregulated inflammation is important, with particular emphasis on cardiovascular disease.
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Atherosclerosis is the result of prolonged and excessive inflammatory processes in the vascular wall, often beginning with inflammatory changes in the endothelium and characterized by expression of adhesion molecules.
“Accumulating evidence indicates that AS is the result of a prolonged and excessive inflammatory processes in the vascular wall, which often begins with inflammatory changes in the endothelium and is characterized by the expression of adhesion molecules.2, 3”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [2]
Inflammation participates centrally in all stages of AS from initial lesion to end-stage thrombotic complications.
“Inflammation participates centrally in all stages of AS from the initial lesion to end‐stage thrombotic complications.”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [2]
The process of AS often begins with inflammatory changes in the endothelium, characterized by expression of adhesion molecules.
“The process often begins with inflammatory changes in the endothelium, characterized by expression of adhesion molecules.2, 3”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [2]
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“Recently, pathways involved in the resolution of inflammation have garnered attention for their potential contribution to non-resolving inflammatory responses [4,5].”
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- Authors
- Maskrey, B. H., Megson, I. L., Whitfield, P. D., & Rossi, A. G.
- Affiliations
- Centre for Inflammation Research (GB)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2011-05
- Volume
- 31
- Issue
- 5
- Pages
- 1001-1006
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W1996733544
- Cited by
- 177
- References
- 58
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 6 · 2023: 9 · 2022: 12 · 2021: 7 · 2020: 8 · 2019: 12 · 2018: 12 · 2017: 13 · 2016: 19 · 2015: 19 · 2014: 14 · 2013: 10 · 2012: 16
- FWCI
- 6.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- inflammation resolution, chronic inflammation, innate immunity, apoptosis, atherosclerosis, cardiovascular disease, tissue repair, dysregulated inflammation
- MeSH terms
- Animals, Anti-Inflammatory Agents, Cardiovascular Diseases, Granulocytes, Humans, Inflammation, Nitric Oxide, Lipid Peroxidation, Signal Transduction, Apoptosis, Inflammation Mediators, Cyclin-Dependent Kinases
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