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Inflammatory pathways in atherosclerosis and acute coronary syndromes
1Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115, USA. jplutzky@rics.bwh.harvard.edu
Insights
Atherosclerosis is a chronic inflammatory disease involving immune cells and proteins. Targeting inflammation may reduce cardiovascular risk, heralding a new era in cardiovascular medicine.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Inflammation Biology
Background:
- Atherosclerosis is a chronic inflammatory disease.
- Inflammatory cells (T cells, monocytes, macrophages) and proteins (cytokines, chemokines) play key roles.
- Vascular cells contribute through inflammatory responses like adhesion molecule expression.
Purpose of the Study:
- To review the role of inflammation in atherosclerosis.
- To identify proteins that predict cardiovascular risk.
- To explore inflammation as a therapeutic target.
Main Methods:
- Review of evidence from broad studies on atherosclerosis.
- Identification of key inflammatory markers.
- Analysis of therapeutic interventions targeting inflammation.
Main Results:
- C-reactive protein, tumor necrosis factor-alpha, and interleukin-6 are widely studied risk predictors.
- Statins, ACE inhibitors, and PPAR ligands may reduce cardiovascular risk partly via anti-inflammatory effects.
- Inflammation is a central mechanism in atherosclerosis progression and complications.
Conclusions:
- Inflammation is integral to atherosclerosis pathogenesis and progression.
- Biomarkers of inflammation hold predictive value for cardiovascular risk.
- Targeting inflammation represents a promising therapeutic strategy in cardiovascular medicine.
Abstract:
Evidence from a broad range of studies demonstrates that atherosclerosis is a chronic disease that, from its origins to its ultimate complications, involves inflammatory cells (T cells, monocytes, macrophages), inflammatory proteins (cytokines, chemokines), and inflammatory responses from vascular cells (endothelial cell expression of adhesion molecules). Investigators have identified a variety of proteins whose levels might predict cardiovascular risk. Of these candidates, C-reactive protein, tumor necrosis factor-alpha, and interleukin-6 have been most widely studied. There is also the prospect of inflammation as a therapeutic target, with investigators currently debating to what extent the decrease in cardiovascular risk seen with statins, angiotensin-converting enzyme inhibitors, and peroxisome proliferator-activated receptor ligands derives from changes in inflammatory parameters. These advances in basic and clinical science have placed us on a threshold of a new era in cardiovascular medicine.