Konstantinos Mourouzis1, Evangelos Oikonomou1, Gerasimos Siasos1, Sotiris Tsalamadris1, Georgia Vogiatzi1, Alexios Antonopoulos1, Petros Fountoulakis1, Athina Goliopoulou1, Spyridon Papaioannou1, Dimitris Tousoulis1.
Abstract
BACKGROUND: Over the last decades, the role of inflammation and immune system activation in the initiation and progression of coronary artery disease (CAD) has been established.
OBJECTIVES: The study aimed to present the interplay between cytokines and their actions preceding and shortly after ACS.
METHODS: We searched in a systemic manner the most relevant articles to the topic of inflammation, cytokines, vulnerable plaque and myocardial infarction in MEDLINE, COCHRANE and EMBASE databases.
RESULTS: Different classes of cytokines (intereleukin [IL]-1 family, Tumor necrosis factor-alpha (TNF-α) family, chemokines, adipokines, interferons) are implicated in the entire process leading to destabilization of the atherosclerotic plaque, and consequently, to the incidence of myocardial infarction. Especially IL-1 and TNF-α family are involved in inflammatory cell accumulation, vulnerable plaque formation, platelet aggregation, cardiomyocyte apoptosis and adverse remodeling following the myocardial infarction. Several cytokines such as IL-6, adiponectin, interferon-γ, appear with significant prognostic value in ACS patients. Thus, research interest focuses on the modulation of inflammation in ACS to improve clinical outcomes.
CONCLUSION: Understanding the unique characteristics that accompany each cytokine-cytokine receptor interaction could illuminate the signaling pathways involved in plaque destabilization and indicate future treatment strategies to improve cardiovascular prognosis in ACS patients. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
BACKGROUND: Over the last decades, the role of inflammation and immune system activation in the initiation and progression of coronary artery disease (CAD) has been established.
OBJECTIVES: The study aimed to present the interplay between cytokines and their actions preceding and shortly after ACS.
METHODS: We searched in a systemic manner the most relevant articles to the topic of inflammation, cytokines, vulnerable plaque and myocardial infarction in MEDLINE, COCHRANE and EMBASE databases.
RESULTS: Different classes of cytokines (intereleukin [IL]-1 family, Tumor necrosis factor-alpha (TNF-α) family, chemokines, adipokines, interferons) are implicated in the entire process leading to destabilization of the atherosclerotic plaque, and consequently, to the incidence of myocardial infarction. Especially IL-1 and TNF-α family are involved in inflammatory cell accumulation, vulnerable plaque formation, platelet aggregation, cardiomyocyte apoptosis and adverse remodeling following the myocardial infarction. Several cytokines such as IL-6, adiponectin, interferon-γ, appear with significant prognostic value in ACS patients. Thus, research interest focuses on the modulation of inflammation in ACS to improve clinical outcomes.
CONCLUSION: Understanding the unique characteristics that accompany each cytokine-cytokine receptor interaction could illuminate the signaling pathways involved in plaque destabilization and indicate future treatment strategies to improve cardiovascular prognosis in ACS patients. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities:
Keywords:
Acute coronary syndrome; adipokines; atherosclerosis; cytokines; inflammation; vulnerable plaque
Mesh：
Substances：
Year: 2020
PMID： 32282296 DOI： 10.2174/1381612826666200413082353
Source DB: PubMed Journal: Curr Pharm Des ISSN： 1381-6128 Impact factor: 3.116